To Lizzie and Sue

and to the memory of Dr. Keith Heller, a dear friend and

dedicated colleague
11830 Westline Industrial Drive
St. Louis, Missouri 63146

DENTISTRY, DENTAL PRACTICE, AND 0-7216-0515-X

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 PREFACE TO THE SIXTH EDITION
Change is the only true constant in our uncertain world, and this sixth edition comes into a world
that is very different from that which greeted the fifth edition in 1999. The budget surpluses of that
time have plunged to become record deficits, and as a nation we are ambivalent about a war that may
bring democracy to a troubled land or may drag us into a morass. Most of all, our national mindset
is dominated by the horrors and heroism of September 11, 2001. And what has unpredictable social
change got to do with dentistry? The answer is a great deal, for the dental world, like any other insti-
tution, is part of the overall pattern. If the world is an ecosystem, then changes in population,
income, employment, inflation, and just about everything else will affect dentistry to some extent.

The purpose of this book is to present dentistry and dental practice against the backdrop of social
events: economic, technological, and demographic trends, as well as the distribution of the oral dis-
eases that dental professionals treat and prevent. The pace of change in these areas can be bewilder-
ing, and substantial rewriting of many parts of this book has thus been required. Since the 1999
edition came out, we have seen our health system, based on something called managed care, become
less and less workable. Dentistry in Medicaid is barely visible, “access” has emerged as a major health
issue, and the corporate burden of providing health care for employees is threatening our national
economy. Dentistry cannot be a bystander as these issues continue to demand public attention.
Rather, dentistry needs to understand them as best we can and take its place at the table as a leader in
setting health care policy.

Our guiding principle in this sixth edition is that we lay out the facts on all matters discussed and
interpret them as we see them. We express our opinions, taking care to distinguish opinion from fact,
and leave the reader to develop his or her own views. We subscribe to the view that health is a major
contributor to a higher quality of life rather than an end in itself. We have no doubt that good oral
health significantly improves the quality of life and that the constant improvement of the public’s
oral health is a worthy goal.

The lineage of this book can be traced from the landmark work of Pelton and Wisan’s Dentistry in
Public Health, first published in 1949, up to our fifth edition in 1999. We carry on the tradition in
this sixth edition, which has 30 chapters in five parts, more than ever before. That growth reflects the
expansion of the issues with which dentistry is involved. The first part looks at the dental professions
and the public they serve and deals with ethics, the public-private partnership, public health prac-
tice, and health promotion. Part II deals with the structure and financing of dental practice, types of
personnel in the dental workforce, infection control and mercury safety, and a new chapter on access
to dental care. The chapter on reading the literature is now joined by a new chapter on evidence-
based dentistry. Part III is the nitty-gritty of oral epidemiology, from research designs and survey
methods to the various indexes used to measure oral disease, and Part IV looks at the distribution of
these diseases in the population and the various risk factors associated with them. In conclusion,
Part V deals with the prevention of oral diseases and conditions.

In matters of style, we favor liberal referencing. This gives readers a chance to pursue further the
issues that interest them, and the references give the basis for our interpretation of the more con-
tentious issues. We list more references with potentially contentious issues than with the more
straightforward ones. Although most references reflect current work, we have retained a lot of older
ones to illustrate how issues have developed over time and to show the richness of the dental litera-
ture. We should never forget our roots. As would be expected, a growing number of references are to
sites on the Internet, although we all have mixed feelings about the growing dominance of the
Internet as a source of basic information. On the one hand, it makes information more immediately
available than ever: if knowledge is power, we are all more powerful. On the other hand, Internet
material can be startlingly temporary. Even during the production of this edition, a number of
vii
viii Preface to the Sixth Edition

websites we were using as reference sources simply disappeared. Citing full websites can be
extremely awkward, with URLs running on for two or three lines. When just the home page or sec-
ond-level main page is cited in the quest for a stable reference, readers need enough familiarity with
the Internet to be able to go to the other one or two levels to find the precise table or text statement.
We know the Internet will continue to develop rapidly, although what it will look like in 10 years’
time is anybody’s guess.

We have continued our method of dealing with the gender-specific personal pronoun by making it
feminine in the odd-numbered chapters, masculine in the even-numbered. The “her” of Chapter 1
thus becomes the “his” of Chapter 2. In our frequent use of the term dental professionals, we include
both dental hygienists and dentists as colleagues working together.

Contrasts have to be made at times between how things are done in the richer parts of the world
compared to the poorer. We use the term developed countries, or sometimes industrialized or the
World Bank term of high-income countries, to refer to nations such as the United States, Canada,
most European countries, Australia, New Zealand, and Japan, which have industrial and service-
based economies, high levels of literacy, a large middle class, sophisticated transport systems, and
mass distribution of goods far from their point of origin. By contrast, the developing or low-income
nations are those in which those factors are just beginning to be seen or in which they do not exist at
all. In addition, there are many nations that don’t clearly fit either category but lie somewhere
between the two: well-developed in some areas and less so in others. Without going into details of
world economics, we occasionally use those oversimplified categories of “developed” and “develop-
ing” to illustrate broad differences.

We owe a debt of gratitude to those who have helped us with materials and other information for
this book. In alphabetical order, we thank Patricia Anderson, Pilar Baca, Eugenio Beltrán-Aguilar,
Robert (Skip) Collins, Steve Levy, Thom Marthaler, Kevin O’Brien, Jim Pittman, Scott Presson,
Woosung Sohn, Scott Tomar, and Helen Whelton. All of these people made our task a little easier,
although we emphasize that responsibility for every word in this book lies with us, and with us
alone.

So who knows what lies ahead for the twenty-first century? We certainly don’t pretend to have the
answers, other than to state the obvious: it will be a challenging and exciting time for dentistry. To
thrive and progress, dental professionals require a mindset that permits them to adapt to changing
circumstances. We hope that this book will help readers to develop that mindset.
Brian A. Burt, BDS, MPH, PhD

Stephen A. Eklund, DDS, MHSA, DrPH

 1 The Professions of Dentistry
and Dental Hygiene
DEVELOPMENT OF THE DENTAL
PROFESSIONS
Dentistry
Dentistry in the Twentieth Century
Dental Hygiene
ORGANIZATION OF THE DENTAL
PROFESSIONS IN THE UNITED STATES
American Dental Association
National Dental Association
Hispanic Dental Association
Dental practice has existed in some form since
the dawn of time, but it is only in comparatively
recent years that its practitioners in the econom-
ically developed nations have achieved the sta-
tus of a profession. In most of the low-income
world, dental practice is still more of a craft. In
countries with a moderate level of economic
development, dentistry exhibits some aspects of
a profession, but not all.
Webster’s dictionary defines a profession as “a
calling requiring specialized knowledge and
often long and intensive academic preparation”
and “the whole body of persons engaged in a
calling.” The definition of professionalism is “the
conduct, aims, or qualities that characterize or
mark a profession or professional person.”
These terse dictionary definitions, however, do
not fully capture the essence of a profession or
of professionalism: commitment to patient
welfare, ethics, and other professional ideals
are not included. Nor are all aspects of profes-
sionalism necessarily high-minded or noble.
Admission to some professional groups can be
based on self-perpetuation rather than public
good, and aspects of “closed shop” practices in
professions have not been uncommon.30
Three models of professionalism have been
described,25 none of which by itself fully char-
acterizes dentistry, although collectively they
Other Groups in Dentistry
FDI World Dental Federation
American Dental Hygienists’ Association
CAREERS IN DENTISTRY AND DENTAL
HYGIENE
Private Practice
Salaried Practice
U.S. Public Health Service
Academia: Dental Education and Research
may do so. The first is the commercial model, in
which dental care is viewed as a commodity
sold by the practitioner. The services are thus
not based primarily on the client’s needs, but
rather on what the client is able or willing to
buy. This rather crass view is distasteful to many,
although there are aspects of it in dental prac-
tice. The second is the guild model, in which
dental care is seen as a privilege with the profes-
sional dominant in practitioner-patient rela-
tions. In the guild model the professional is the
repository of all knowledge and wisdom, the
patient is a passive recipient, and the practi-
tioner has an ethical trust to provide the best-
quality care. This model has probably been
dominant in the United States, although it may
be slowly merging with the third model, the
interactive model, in which dental care is consid-
ered a partnership of equals. In this model,
practitioner and patient jointly determine care
provided through a combination of profes-
sional expertise and patient values.
What are the criteria that characterize a pro-
fession, and how can a profession be distin-
guished from, say, a trade union? The first is the
criterion given in the dictionary definition, a
substantial body of knowledge, a corollary of
which is the obligation to keep that knowledge
up to date through continuing education. The
3
4 Dentistry and the Community
second is self-regulation, a tradition whereby
society delegates to professional groups the
legal responsibility for determining who shall
join them in serving the public and for disci-
plining those members who do not meet the
profession’s requirements. A third and perhaps
the main distinguishing criterion of a profes-
sion is a code of ethics, guidelines for profes-
sional conduct that are rooted in a moral
imperative rather than in law or regulation (see
Chapter 3). A profession sets its own code of
ethics and its own procedures for dealing with
infringements. Taking the various criteria men-
tioned, one can distinguish a profession by the
features listed in Box 1-1.
A health profession can then be defined by
paraphrasing Webster’s definition given earlier:
a calling in the health sciences requiring special-
ized knowledge, and one that meets the other cri-
teria listed. Dentistry meets all the requirements
of a profession. Dental hygiene is usually consid-
ered a profession within dentistry, although for
the most part it is not self-regulating.
DEVELOPMENT OF THE DENTAL
PROFESSIONS
Dentistry
Dental diseases have afflicted the human race
since the dawn of recorded history.22,29
Dentistry, however, has existed as a vocation
only in recent years, historically speaking, and it
was not until modern times that any sort of sci-
entific basis was developed for the care of oral
diseases. One landmark event was the 1728
publication of Pierre Fauchard, Le Chirurgien
Dentiste, ou Traite des Dents, a two-volume
book of more than 800 pages. Fauchard, a
BOX 1-1 Characteristics of a Profession
●
A body of knowledge exists that is constantly being
expanded, updated, and archived in a literature record.
The purpose is constant improvement of the quality of
the profession’s service to individuals and to the
public.
●
Academic preparation is required, carried out in
specialized institutions.
●
The profession and its members accept a lifelong
commitment to continuing education.
Frenchman, is looked upon as a seminal figure
in the evolution of the dental profession. His
work was the first complete treatise on dentistry
published in the Western world, and it remained
an authoritative document for over 100 years.
Fauchard, despite the lack of formal training,
was clearly a first-class empiricist with keen
powers of observation.
Aspiring dentists of the time served as
apprentices. It is worth noting that even the
formal education of G. V. Black, one of the pro-
fession’s most notable nineteenth-century
pioneers, did not exceed 20 months. His intro-
duction to dentistry consisted of “a few weeks”
with one Dr. Speers, who was not considered a
particularly good dentist and whose dental
library consisted of one book.9 Fortunately,
Dr. Black was a true professional and followed
the precept that “a professional person has no
choice other than to be a continuous student.”
The first American dental school was the
Baltimore College of Dental Surgery, later part
of the University of Maryland, established in
1840. The course was 16 weeks in length after a
year or more of apprenticeship. The initial
enrollment was five, of whom two graduated. At
about the same time, the first national profes-
sional dental journal appeared, the American
Journal of Dental Science, and the first national
dental organization, the American Society of
Dental Surgeons, was established. The genesis
of the dental profession in the United States can
thus be dated fairly precisely to the 1840
period. The path of professional progress was
not entirely smooth, however, for the emer-
gence of dentistry as a fledgling profession was
followed by an undignified scramble to open
proprietary dental schools. In the best American
●
Society awards the profession the privilege of self-
regulation, which means determining the requirements
for entering and remaining in the profession, and dealing
with those members who do not meet the requirements.
●
Its members subscribe to a code of ethics drawn up
by the profession itself.
●
The members form organized societies to enhance the
development of the group and its societal mission,
and to serve its individual members.
 1 The Professions of Dentistry and Dental Hygiene
traditions of free enterprise and entrepreneur-
ship, most of these places were run strictly for
profit. In the years before public and profes-
sional regulation, the proprietary schools
turned out thousands of graduates whose pro-
fessional abilities covered the spectrum from
respectable to dreadful.
The anarchic events of the time, however, led
to dentistry’s development in the United States
as a profession separate from medicine, a posi-
tion that has been maintained to the present
day. This separate development actually occurred
more by chance than by deliberate policy, for it
was originally intended that the Baltimore den-
tal school be established within the medical
school. It was not, but only because of lack of
space and internal friction among medical
school faculty. The separation of dentistry from
medicine was standard in the English-speaking
world, Scandinavia, and some other European
countries, but in central and southern Europe,
by contrast, there was a division between stom-
atologists (physicians with specialty training in
clinical dentistry) and dentists, who in this con-
text were second-level providers. This division
of labor is thought not to have benefited oral
health in most of the countries concerned13 and
has been abandoned in most of them as the
European Community moves toward standardi-
zation of professional training. On the other
hand, whether American dentistry benefited
from its evolution on a branch that grew out of
the main medical trunk, rather than being more
closely allied to medicine during its formative
years, can be debated. By the early twenty-first
century, there were signs that dentistry might be
evolving into something closer to the medical
model.
Dentistry in the Twentieth Century
The era of modern dentistry could be said to
date from the closing of the last proprietary
school in 1929, which came shortly after the
landmark Gies report on dental education. Gies
collected information from the dental schools
of the time and concluded that the dental pro-
fession would only progress when dental educa-
tion became university based and subject to the
maintenance of high standards through accredi-
tation. Despite the adoption of Gies’s recom-
mendations, however, dental practice during
the economic depression of the 1930s was
5
largely a matter of survival, with few patients
able to afford dental care. World War II fol-
lowed, during which dentists, along with other
health professionals, were drafted into the
armed forces. As part of the national mobiliza-
tion for the war effort, American dental schools
compressed the curriculum of four academic
years into three calendar years. This expedient
was dropped when the war ended in 1945,
although it was flirted with again for a short
time in the 1970s.
The 1930s and 1940s were a hard time for
dental education. The teaching of basic science
was often perfunctory and the emphasis in the
clinical sciences was almost entirely on restora-
tive dentistry and prosthetics. Subjects such as
radiology, oral diagnosis, endodontics, peri-
odontics, and pediatric dentistry were neglected
in many dental schools, and full-time faculty
were the exception rather than the rule. There
were few educational programs for the prepara-
tion of specialists, and the few that did exist var-
ied in quality and length.20 One of the few
bright spots during this difficult period was the
beginning of the first controlled water fluorida-
tion projects in 1945 (see Chapter 25).
With a rapidly expanding postwar economy
and population, added to accelerating techno-
logic growth and a spirit of optimism, dentistry
entered what some saw as a golden age during
the 1950s. New dental materials expanded
treatment horizons, and the arrival of the high-
speed air-turbine engine in 1957 revolutionized
dental practice. Dental research, stimulated by
the establishment of the National Institute of
Dental Research (now the National Institute
of Dental and Craniofacial Research) in 1948,
grew rapidly, and the publication of The Survey
of Dentistry in 196118 led to improvements in
education and practice. Stagnating dental
schools were revitalized with the passage of the
Health Professions Educational Assistance Act
in 1963. This act authorized federal funds for
construction and student aid. Later renewals in
1971 and 1976 included per capita funding to
support the basic instructional program. In the
15 years from 1963 to 1978, the addition of fed-
eral monies to state, local, and private sources
spurred the reconstruction of the entire physical
plant of dental education.16 New schools were
built too; the 39 dental schools in 1930 had
increased to 59 by 1980.1
6 Dentistry and the Community
The 1960s and 1970s saw the emergence of
comprehensive care, growth in use of auxil-
iaries, the beginnings of prepaid dental insur-
ance, and the development of a community
outlook in dentistry. Growth in the number
of dentists and in dental business was sharp, in
retrospect perhaps too sharp. The economic
downturn following the Vietnam War (1964–75),
added to the decline in dental caries among
children (see Chapter 20), led to a growing per-
ception of an oversupply of dentists, despite
increasing public utilization of services (see
Chapter 2) and continued growth of dental
insurance (see Chapter 7). During the 1980s,
enrollment in dental schools dropped substan-
tially from its peak during 1977–79 and rose
only a little from these levels through the mid-
1990s (see Chapter 8). In response, seven dental
schools closed during this period (Emory,
Fairleigh Dickinson, Georgetown, Loyola of
Chicago, Northwestern, Oral Roberts, Washington
University). Applications to dental schools
picked up again in the late 1990s, and new den-
tal schools opened in Arizona, Florida, and
Nevada. In the early twenty-first century there
were 56 dental schools in the United States.6
In the new century, the major oral diseases
are better controlled than ever, and dental prac-
tice will evolve accordingly. Research in molecu-
lar biology is promising a new understanding of
many diseases, including those oral diseases
that currently are poorly understood and that to
date have not been treated in dental practice.
Other features that will shape dental practice in
the new century are the changing demographic
profile (see Chapter 2), disease patterns (see
Chapters 19-23), developments in dental
insurance (see Chapter 7), and new restorative
materials. Infection-control procedures and
their associated regulations had become stan-
dard practice by the 1990s (see Chapter 10).
Dental Hygiene
Dr. Alfred Fones, an 1890 graduate of the New
York College of Dentistry, developed a tech-
nique for scaling and polishing teeth and also
taught his patients to carry out home-care
procedures. By 1906, acting under the preven-
tive dictum that “a clean tooth never decays,”
Dr. Fones was sure that the oral health of
his patients was improved through his oral pro-
phylactic practices. He trained his assistant to
practice dental hygiene, and in 1907 he was
instrumental in having dental hygiene legally
recognized in Connecticut as an adjunct to den-
tal practice. Fones went on to establish the first
school of dental hygiene in 1913. Accepting
only “young ladies of good character,” the
school was located in a carriage house on the
grounds of the Fones residence.23 Connecticut
passed legislation specifically describing the
practice of dental hygiene in 1916. Ten states
had similar legislation in place by 1920, and the
total rose to 34 in 1935. Not until 1951, how-
ever, did the practice acts of all states, the
District of Columbia, and the Commonwealth
of Puerto Rico include provisions for the prac-
tice of dental hygiene.14
This leisurely development of dental hygiene
was largely tied to the development of dental
schools. In 1945, of the 16 dental hygiene pro-
grams then in existence, 13 were associated with
schools of dentistry. By 1974, however, only 37
of 158 were so affiliated. The explosive growth
after 1960 mostly took place in junior and com-
munity colleges,14 stimulated by federal funds
for vocational-technical education in health
occupation training centers. The numbers of
training programs, especially the 2-year pro-
grams, fluctuated with demand for hygienists
and the availability of federal funding. By 1980
the number of programs was 204; it was down to
190 by the end of the 1980s and back over 250
again early in the new century (see Chapter 8).
During the first 30 years of dental hygiene
education, there was no uniformity in either
prerequisites or curriculum. These variations
were due to differences in state licensing acts,
problems of integrating a 2-year clinical pro-
gram into a 4-year baccalaureate degree curricu-
lum, and the lack of nationally approved
standards. The latter problem was remedied in
1947, when the Council on Dental Education
of the American Dental Association (ADA)
adopted the first accreditation requirements for
dental hygiene schools. In 1952, the council
began an active program in accreditation of
dental hygiene schools. The requirements
developed then still essentially stand today.
For training in dental hygiene, a 2-year
curriculum must meet the standards of the
ADA’s Commission on Dental Accreditation. In
all states except Alabama, which recognizes
preceptorship, the completion of an accredited
 1 The Professions of Dentistry and Dental Hygiene
2-year curriculum is the minimum requirement
for admittance to licensure examination by a
state dental board. An individual enrolled in a
4-year baccalaureate degree program must also
meet university standards for that degree. Many
dental hygienists earn advanced degrees (MS,
MPH, PhD, DrPH), for which the requirements
of the university’s graduate school also must be
met.
ORGANIZATION OF THE DENTAL
PROFESSIONS IN THE UNITED
STATES
The legal basis for dental practice in the United
States is the dental practice act in each state. It is
not a federal matter. The effect of these acts on
dental practice is discussed more fully in
Chapter 8. Here we look at the professional
organizations in dentistry.
American Dental Association
The ADA was founded in 1859 by 26 dentists
meeting at Niagara Falls. Today it claims some
147,000 members,2 about 70% of the nation’s
dentists. It is easily the largest and most influen-
tial dental organization in the country. It
operates on a tripartite basis, meaning that mem-
bers must join the local society (a component),
the state or territorial society (a constituent), and
the national ADA; they cannot be members of
just one or two (with the exception of students
and dentists in the federal services). There are 53
constituent societies and 545 components.3
The tripartite system has been in place since
1913, when it was modeled on the structure of
BOX 1-2 Three Primary Areas in Which the American Dental Association Serves Its Members and, Indirectly,
the Public
1. Facilitating the growth and dissemination of scientific
information. This is done by holding scientific
meetings at the local, state, and national levels and is
enhanced by the publication of a variety of scientific
journals. The Internet continues to emerge as an ever
more important medium of information exchange.
2. Establishing standards, such as accreditation of
professional schools for dentists, dental hygienists,
dental assistants, and dental laboratory technicians.
7
the American Medical Association. The purpose
of adopting the tripartite structure was to unify
a profession that at the time was highly frag-
mented and to improve efficiency through
avoiding duplication of effort. The tripartite
structure was challenged in 1972 by four
Arizona dentists, who argued that by requiring
membership at all levels the ADA had instituted
an illegal arrangement. The district court ruled
against the dentists in 1980, stating that the
membership requirement did not suppress
competition between dentists, and it also dis-
agreed with the charge that the associations or
their members held a monopoly on the practice
of dentistry in Arizona. The decision was
upheld in the court of appeals in 1982,21 and
subsequent challenges to the tripartite structure
have been similarly unsuccessful.
Dentists apply for membership in a compo-
nent society, which represents a county, a group
of counties, or a large city. If accepted at this
local level, the dentist automatically becomes a
member of the state dental society and of the
ADA. Traditionally membership standards have
included graduation from an accredited dental
school, a license to practice in the jurisdiction,
and “good moral standing,” a vague term that
has been interpreted in various ways.
ADA membership provides access to a num-
ber of fringe benefits that are important to a self-
employed practitioner, such as group insurance
plans and the availability of expert consultative
services. It also serves its members, and indirectly
the public, by the activities shown in Box 1-2.
The ADA is cohesive and well organized. Its
ultimate governing body is the 427-member
Standards are also established for materials, drugs, and
devices used by dentists in practice and for some
products offered for sale to the public. These standards
are established by having experts in specialized fields
serve as members of reviewing councils and committees.
3. Obtaining a consensus among the profession on
major issues and transmitting this consensus to
government agencies and others concerned with
establishing policies for public health.
8 Dentistry and the Community
House of Delegates, which comprises elected
representatives from the 50 states, the District of
Columbia, the Commonwealth of Puerto Rico,
the Virgin Islands, five federal dental services
(Air Force, Army, Navy, U.S. Public Health
Service, Department of Veterans Affairs), and
the American Student Dental Association.3 As
in the U.S. House of Representatives, state dele-
gations are proportional to state dental popula-
tions; they range from 1 delegate (the Virgin
Islands) to California’s 47.
The Board of Trustees, charged with day-to-
day responsibility for the ADA’s operations, is
made up of a trustee from each of 17 geographic
districts of roughly equal numbers of dentists,
plus the president, president-elect, and first and
second vice-presidents. The Board reports on its
activities to the House of Delegates. It also
reviews most resolutions on their way to the
House and recommends what action should be
taken on them.7
The House of Delegates conducts business
once a year for 5 days during the annual session.
Resolutions may be introduced by the Board of
Trustees, the ADA’s commissions and councils,
the trustee districts, constituent and component
societies, or directly by delegates. Resolutions,
along with supporting documentation, are
referred for hearing to one of seven reference
committees. Depending on the issues in any
given year, special (generally single-issue) com-
mittees may be established to study particular
questions in depth. The hearings of the refer-
ence committees are open to all members of the
association. At these meetings members are
encouraged to speak their minds and advise the
House of Delegates of their positions on
specific issues or on the status of the association
as a whole. The reference committees prepare
reports that are transmitted to the House of
Delegates. As the House considers the issues,
it usually has the original resolution and
background report, the comments and recom-
mendations of the Board of Trustees, and the
report and recommendations of the reference
committee. On the basis of this information,
the House acts to adopt, defeat, amend, substi-
tute, or refer.
The ADA has long been keenly aware of the
public image of dentistry and has conducted
many campaigns to promote it. Children’s
Dental Health Month, which grew from an
original 1-week campaign and is held in
February each year, is the oldest annual public
relations exercise. The ADA notes that on its
Give Kids a Smile! Day in February 2003 thou-
sands of children received needed dental treat-
ment from dentists who donated their services.4
The impact of these campaigns is discussed in
Chapter 5.
Dentistry just might be a bit overly preoccu-
pied with its image, for many public opinion
polls show that the public consistently ranks
dentists high in terms of professional trust.12
The sometimes prickly sensitivity of dentistry to
its image is seen in the chorus of complaints
when dentists are portrayed in movies or TV as
bumbling, obsessive, or sadistic, or when news-
casters refer to “doctors and dentists.” (One that
gets under our skin is reference to “medical
treatment” and “dental work.”) These things
can grate at times, but they seem to be part of
the territory. When they are viewed in the per-
spective of how all professions are treated in the
media, it is doubtful if any real harm is done by
media imagery.
National Dental Association
In past years, rigid attitudes on racial separation
meant that most component dental societies of
the ADA did not accept dentists of African-
American origin. African-American dentists
therefore went their own way and in 1913 estab-
lished the National Dental Association (NDA).
Those days of nonacceptance are now happily
gone; in recent years both the ADA and the NDA
have stated that their objective is complete inte-
gration of the dental profession. White dentists
now belong to the NDA and African-American
dentists belong to the ADA, and there is a good
cooperative relationship between the two
organizations. They continue to exist separately,
however, for traditional reasons. Today the NDA
has some 7000 dentist members, and it also has
acted as the umbrella organization for the
National Dental Hygienists’ Association since
1963.24
Perhaps more so than the ADA, the NDA
has been a consistent champion of efforts to
improve the health status of those in our society
who are most often underserved by the health
care system. Such groups include racial and eth-
nic minorities, children, the indigent, the eld-
erly, and the disabled.
 1 The Professions of Dentistry and Dental Hygiene
Hispanic Dental Association
Established in 1990, the Hispanic Dental
Association (HDA) represents the interests of
both Hispanic professionals and patients.17
This active organization already has some
15,000 members, a well-established organiza-
tional structure, and a number of affiliated
groups throughout the country. The mission of
the HDA is to improve the oral health of the
Hispanic community, and to that end it spon-
sors continuing education and oral health pro-
motional activities directed at the Hispanic
population. Since Hispanics are the fastest-
growing ethnic minority in the United States
(see Chapter 2), the HDA is confidently looking
forward to increased growth.
Other Groups in Dentistry
Beyond the major national organizations and
their constituent and component societies, each
specialty group has its own organization:
the American Academy of Periodontology, the
American Association of Oral and Maxillofacial
Surgeons, the American Association of Public
Health Dentistry, and so on. These specialty
organizations serve as sponsors of the specialty-
certifying bodies whose role is discussed in
Chapter 8. At another level still, there are myr-
iad study clubs and groups of dentists brought
together by common interests.
FDI World Dental Federation
Practically every country with a recognizable
dental profession has a working national organi-
zation, an equivalent of the ADA, although
no other national dental association has
resources as extensive as those of the ADA. On
the international scene, the FDI World Dental
Federation is an organization of national dental
associations. The name needs some explanation.
Formed in the early twentieth century as a loose
grouping of several European national associa-
tions, the organization was first known as the
Fédération Dentaire Internationale (French for
International Dental Federation, hence the
acronym FDI). In its early years it was a distinctly
European organization, but with global expan-
sion it changed its name to the World Dental
Federation. The acronym FDI was so well known
by that time, however, that it was kept as part of
the title of the organization. FDI now represents
9
over 150 national dental organizations and
35 other international organizations, encom-
passing altogether over 700,000 dentists.15
Headquartered in London for years, the FDI is
now based at Ferney-Voltaire, France, the
same city where the World Medical Association31
is located and close to the World Health
Organization’s home in Geneva, Switzerland.
The FDI has a full-time executive secretary, a
large staff, and a structure that resembles that of
the United Nations. Its work is both scientific
and political. Its technical committees bring
international experts together to develop state-
of-the-art reports and recommendations for fur-
ther action. Politically, the FDI has been helpful
in the development of the dental professions
and dental care services in many countries where
the local profession has little political clout. It
publishes the International Dental Journal, a
respected journal in the dental literature.
American Dental Hygienists’ Association
In 1923, 46 dental hygienists from 11 states met
in Cleveland, Ohio, to organize the American
Dental Hygienists’ Association (ADHA). They
received strong support from the dental profes-
sion. While early growth was not spectacular, in
the 1925–45 period, active membership went
from several hundred to about 2000. In the next
10 years (1945–55) membership more than
doubled to nearly 4400, and growth has been
spectacular since then. In 2003 the ADHA repre-
sented the interests of more than 120,000 regis-
tered dental hygienists.8
The organization of the ADHA closely paral-
lels that of the ADA. There are seven classifica-
tions of membership (including student
membership for a modest fee), but the basic
category of “active” membership must be held
through constituent and component associa-
tions if such exist. There are 375 component
(local) associations. The House of Delegates
meets once a year and has all legislative and
policy-making powers for the association. The
Board of Trustees is composed of the elective
officers (except the Speaker of the House), 12
trustees, and the immediate past president, and
has responsibility for supervising the day-to-day
operations. It reviews reports and makes recom-
mendations and relates all of its activities to the
House. The Journal of the American Dental
Hygienists’ Association was established in 1927
10 Dentistry and the Community
and became the Journal of Dental Hygiene in
1988.
CAREERS IN DENTISTRY
AND DENTAL HYGIENE
Private Practice
Private practice, in which the dentist invests
capital into land, buildings, equipment, and
furnishings and in turn seeks to attract patients
who will pay for dental services, is the primary
career choice for most dentists in the United
States. Private practice is a small business, and
so from the career perspective it has all the
advantages and disadvantages of small business
operation.
The advantages are considerable. A dentist
has an almost unlimited choice of where to
locate a practice (provided of course that she is
licensed to practice in the chosen state). Other
advantages are usually a good income, high sta-
tus in the community, and the freedom that
comes from being one’s own boss. Autonomy,
in work practices as well as in selection of treat-
ment options, continues to be the bedrock
value of private practice.10 This is to be expected,
since it fits well with American cultural values.11
Private practice also brings the satisfaction of
knowing that the profession is generally held in
high esteem by the public.
Disadvantages of private practice also relate
to the small business aspects: overhead costs for
utilities, malpractice insurance, disability insur-
ance, staff benefits, equipment maintenance;
retirement planning. The need to adhere to vari-
ous government regulations also absorbs some
effort. Dental practice is highly physical in
nature, and conditions that are only an incon-
venience in many occupations, such as mild
arthritis, a bad back, or failing eyesight, can be
career threatening for a dental practitioner.
An associate in an established practice is
usually paid by salary, or salary plus percentage
of gross production. These arrangements allow
skills to be sharpened before the practitioner
establishes her own practice and can lead to
buying into an established practice. Partnership
too can ease the financial burden of starting
practice, and so can entering a group practice.
Partnerships can provide more flexibility in
practice patterns than does solo practice, but
partners setting out together should be sure
that they are of the right temperament to make
joint decisions and that the personalities
involved are mutually compatible. An unhappy
business partnership can be as emotionally
traumatic and financially devastating as a bro-
ken marriage.
Dental specialists generally earn higher
incomes than generalists. Achievement of spe-
cialist status requires at least an extra 2 years of
education beyond dental school, followed by
specialty board examinations (see Chapter 8).
For specialists, the process of choosing a prac-
tice location parallels that for general practi-
tioners, with two important exceptions. First,
the choice usually is limited to the larger popu-
lation centers; second, the referral potential of
the practitioners in the area, as well as the num-
ber of specialists located there, must be
assessed. In a specialty practice, the supply of
patients is dependent primarily on referrals
from general practitioners. When the general
practitioners are all mature dentists with busy,
established practices, they will usually refer
patients more readily than will younger general-
ists attempting to establish their own practices.
In the latter instance, referrals may be few and
limited to the most extreme problems. The
choices for the two types of specialists who usu-
ally work only in salaried positions, oral pathol-
ogists and public health dentists, are limited by
positions available.
Colorado is the only state that permits inde-
pendent practice of dental hygiene, although
only a few hygienists established their own
practices there after the 1986 law that permitted
independent practice. Most hygienists, in
Colorado as elsewhere, begin their careers treat-
ing patients in the offices of private dental prac-
titioners. They are either reimbursed on a
straight salaried basis or paid a combination of
salary and commission.
Salaried Practice
The advantages and disadvantages of salaried
practice, like those of private practice, are most
related to whether the dentist is temperamentally
comfortable in an organization as opposed to
being a private entrepreneur. Even if a new gradu-
ate does not wish to stay in salaried service
permanently, it is often a good place to start.
Advantages include the opportunity to reduce
dental school debts before incurring more,
 1 The Professions of Dentistry and Dental Hygiene
an immediate specified income, a chance to
improve clinical skills, and time to think about
careers before becoming “locked in” to a practice.
However, for some dentists salaried practice
appeals as a life career. A reasonably good salary
(although not as high as peak earnings in pri-
vate practice), fringe benefits such as health and
disability insurance, liability coverage, a retire-
ment plan, paid vacation time, and freedom
from the overhead costs and day-to-day worries
of private practice can combine to make
the long-term financial prospects of salaried
employment attractive. Some organizations
employing dentists provide opportunities for
continuing education.
For the new dentist interested in general
practice, a general practice residency offers a
form of short-term salaried practice that com-
bines advanced educational opportunities with
the ability to earn. There are over 300 general
practice residencies and advanced general den-
tistry programs accredited by the ADA, all last-
ing 12 or 24 months and offering adequate
stipends. They generally include rotations
through such areas as medicine, emergency
care, anesthesia, and various special areas of
clinical dentistry. This excellent clinical experi-
ence is broadened even further when general
practice residencies include some public health
perspectives (see Chapter 4).
U.S. Public Health Service
Dentists in the U.S. Public Health Service
(USPHS), a component of the Department of
Health and Human Services, serve as commis-
sioned officers of the federal government and
enjoy essentially the same pay, rank, and privi-
leges as their counterparts in the armed services.
The USPHS’s broad mission relates to the
health of the entire nation, in recognition of
which its chief officer is commissioned as
Surgeon General of the United States. The
USPHS carries out major responsibilities in
health research (principally through the
National Institutes of Health) and in the pro-
motion of health through public health efforts.
Clinical care is provided primarily to merchant
seamen, the Coast Guard, American Indians
and Alaska Natives, and residents of federal
prisons. USPHS dental officers serve in a wide
variety of assignments in all states. The clinics of
the Indian Health Service, for example, extend
11
from Point Barrow, Alaska (the farthest north-
ern point of the United States above the Arctic
Circle), to Arizona just north of the Mexican
border. Although the USPHS is the oldest
health service of the federal government, begin-
ning as the Marine Hospital Service in 1798 and
with its Commissioned Corps dating from
1873, it remained relatively unknown to the
public before Surgeon General C. Everett Koop
gave it high visibility during his campaigns
against smoking and in favor of education on
acquired immunodeficiency syndrome during
the 1980s.19 In more recent years, the release of
the Surgeon General’s report on oral health in
America26 and the subsequent call to action27
has thrust the USPHS into an unaccustomed
position of prominence in dentistry.
Other major federal dental services are the
dental corps of the Army, Navy (which also
serves the Marine Corps), and Air Force.
Availability of positions varies with the degree of
military activity, although some openings are
usually present at any given time. The dentist in
the armed services receives all the advantages of
a service career: a reasonably good income, gen-
erous fringe benefits, usually excellent clinical
facilities, and a chance to receive graduate educa-
tion funded by the service. Dentists serve on mil-
itary bases in the United States and overseas. In
the Navy, duty is also available on some ships.
Another major federal dental service, that in
the Department of Veterans Affairs (previously
the Veterans Administration, and hence still
referred to as the VA), was established in 1920
to improve services to veterans of American
wars. It is a major participant in postdoctoral
dental education and it offers, in addition to
specialty programs, more than half of the gen-
eral practice residencies available in the federal
services. Many VA institutions are affiliated with
dental schools. Care is provided in VA hospitals
and outpatient clinics. Occasionally it is pur-
chased from private practitioners. Like all fed-
eral dental programs, the VA program offers
equal employment opportunities for male and
female dentists. Sometimes the VA has been
able to accommodate married couples when
both are health professionals.
For hygienists, expanded opportunities in
the federal service are available for those with a
degree of MPH (Master of Public Health).
A number of hygienists with this degree have
12 Dentistry and the Community
advanced into leadership positions. Civilian
hygienists are employed in the Army, Navy, and
Air Force, although a major share of clinical
procedures ordinarily performed by hygienists
are carried out by specially trained enlisted
personnel.
Outside of the federal dental services there
are other opportunities for salaried employ-
ment. Although the number of state dental
directorships has declined in the twenty-first
century, usually falling victim to state budget
crunches, most states still maintain this post.
Most are filled by a dentist or hygienist with
advanced training in public health, most com-
monly the MPH degree. Dentists and dental
hygienists without advanced training are also
employed by state and local health depart-
ments, group dental practices, prepaid dental
programs, industry-sponsored clinics, and insti-
tutions such as hospitals, prisons, schools for
the mentally retarded, and homes for the men-
tally ill. These positions may involve public
health and administrative activities, clinical
practice, or a combination of both.
Academia: Dental Education
and Research
Dental schools, as noted earlier in this chapter,
used to be staffed largely by part-time faculty
whose primary task was to grade students’ clini-
cal treatment. Academic careers have evolved,
however, and the emphasis now is on full-time
teachers and researchers. The ability to conduct
independent research has become a major crite-
rion for an academic career because research
grant funds increasingly form an important part
of a school’s budget.
An advanced degree is more or less mandatory
for the new dentist or hygienist who is thinking
of an academic career. The most common is the
MS (Master of Science), the usual 2-year degree
taken to fulfill specialty training requirements,
which mixes advanced clinical training with
some research training. Those who want to make
their careers in research need doctoral-level train-
ing in the philosophy and methods of research
through the degrees of PhD (Doctor of
Philosophy), DrPH (Doctor of Public Health), or
ScD (Doctor of Science). The National Institute
of Dental and Craniofacial Research in Bethesda,
Maryland, has information on research training
programs that it supports.28
Academic positions for dental professionals
with advanced degrees have attractive salaries
and fringe benefits. They can be intellectually
demanding, and university politics can be
just as vigorous as politics anywhere else.
The future of dentistry rests with its dental
education institutions and research institutes,
and in the early twenty-first century the short-
age of dental faculty was becoming an issue of
some concern.5 Those employed in these insti-
tutions have the rewards and challenges of
being on the cutting edge of new developments,
of interacting with talented fellow faculty
members, and of relating to students who
represent the future.
REFERENCES
1. American Dental Association. Summary of the
1979–1980 annual report on dental education. J Am
Dent Assoc 1980;100:926-30.
2. American Dental Association. About the ADA, website:
http://www.ada.org/ada/about/index.asp. Accessed
October 26, 2003.
3. American Dental Association. Background on the
American Dental Association, website: http://www.ada.
org/ada/about/ada_background.asp. Accessed October
26, 2003.
4. American Dental Association. Give Kids a Smile!, web-
site: http://www.ada.org/prof/events/featured/gkas/
gkas_background.asp. Accessed October 26, 2003.
5. American Dental Education Association. Faculty short-
ages challenge dental education, and, thus, dentistry:
What is being done?, website: https://www2.adea.org/
adcn/FacultyShortages.pdf. Accessed October 26,
2003.
6. American Dental Education Association. Links to dental
schools and allied education programs, website:
http://www.adea.org/links/default.htm. Accessed October
26, 2003.
7. American Dental Association, House of Delegates.
Structure and function of the ADA’s policy-making
body. J Am Dent Assoc 1976;93:708-12.
8. American Dental Hygienists’ Association, website:
http://www.adha.org/aboutadha/profile.htm. Accessed
September 5, 2003.
9. Bremner MDK. The story of dentistry; from the dawn of
civilization to the present. 3rd ed. Brooklyn NY: Dental
Items of Interest, 1954.
10. Burgess K, Ruesch JD, Mikkelsen MC, Wagner KS. ADA
members weigh in on critical issues. J Am Dent Assoc
2003;134:103-7.
11. Chambers DW. Work. J Am Coll Dentists 2002;
69:38-41.
12. DiMatteo MR, McBride CA, Shugars DA, O’Neill EH.
Public attitudes towards dentists: A U.S. household sur-
vey. J Am Dent Assoc 1995;126:1563-70.
13. Ennis J. The story of the Fédération Dentaire Inter-
nationale. London: The Federation, 1967.
 1 The Professions of Dentistry and Dental Hygiene
14. Fales MJH. History of dental hygiene education in the
United States, 1913 to 1975 [dissertation]. Ann Arbor
MI: University of Michigan, 1975.
15. FDI World Dental Federation, website: http://www.
fdiworldental.org. Accessed September 5, 2003.
16. Galagan DJ. Back from the brink: How and why
U.S. dental schools were rebuilt. Dent Surv 1978;54:
14-8.
17. Hispanic Dental Association, website: http://
www.hdassoc.org/site/epage/8138_351.htm. Accessed
September 4, 2003.
18. Hollinshead BS. The survey of dentistry: The final
report. Washington DC: American Council on
Education, 1961.
19. Koop CE, Ginzburg HM. The revitalization of the
Public Health Service Commissioned Corps. Public
Health Rep 1989;104:105-10.
20. Mann WR. Dental education. In: Hollinshead BS.
The survey of dentistry; the final report. Washington
DC: American Council on Education, 1961:
239–422.
21. McCann D. Tripartite system: Working together for a
common goal. J Am Dent Assoc 1989;119:241–7.
22. Moore WJ, Corbett ME. The distribution of dental
caries in ancient British populations. II. Iron Age,
Romano-British and mediaeval periods. Caries Res
1973;7:139-53.
13
23. Motley WE. Ethics, jurisprudence, and history for the
dental hygienist. 3rd ed. Philadelphia PA: Lea and
Febiger, 1976.
24. National Dental Association. About us, website:
http://www.ndaonline.org/aboutus.htm. Accessed
September 4, 2003.
25. Ozar DT. Three models of professionalism and profes-
sional obligation in dentistry. J Am Dent Assoc
1985;110:173-7.
26. US Public Health Service. Oral health in America:
A report of the Surgeon General. Rockville MD:
National Institutes of Health, 2000.
27. US Public Health Service. A national call to action to
promote oral health. NIH Publication No. 03-5303.
Rockville MD: National Institutes of Health, 2003.
28. US Public Health Service, National Institute of Dental
and Craniofacial Research. Research, website: http://
www.nidr.nih.gov/research/. Accessed October 26,
2003.
29. Weinberger BH. An introduction to the history of den-
tistry, with medical and dental chronology and biblio-
graphic data. St. Louis: Mosby, 1948.
30. Wolfenden. What makes a profession? Br Dent J
1975;139:61-5.
31. World Medical Association. Policy: Introduction and
history, website: http://www.wma.net/e/policy/index.
htm. Accessed November 6, 2003.
 2 The Public Served by Dentistry
POPULATION OF THE UNITED STATES
Population Size and Growth
Age Distribution
Geographic Distribution
Racial and Ethnic Composition
Economic Distribution
Summary of Population Trends
UTILIZATION OF DENTAL SERVICES
Annual Dental Attendance
FACTORS ASSOCIATED WITH THE USE
OF DENTAL SERVICES
Gender
Dentistry exists to serve the public. Many aspects
of that broad statement will be examined
throughout this book, and in this chapter we
start by looking at the structure of the U.S. pop-
ulation. The age distribution of the population,
its ethnic makeup, and its geographic distribu-
tion within the country all profoundly affect the
practice of dentistry. We then look at the pub-
lic’s use of dental services and the factors that
affect that use.
POPULATION OF THE UNITED STATES
Population Size and Growth
In the decennial census of 2000, the population
of the United States was over 281 million, about
4.6% of the world’s population. By 2004 the
population had exceeded 292 million.10
Life expectancy around the beginning of the
twenty-first century reached 76.5 years. Women
live longer than men on average, and the high-
est life expectancy was among white women, at
79.9 years. They were followed by African-
American women at 74.7 years, white men
at 74.3 years, and African-American men at
67.2 years.12 Life expectancy continues to
increase steadily and is expected to keep on
14
Age
Socioeconomic Status
Race and Ethnicity
Geographic Location
General Health
Dental Insurance
FUTURE USE OF DENTAL SERVICES
SUMMARY
increasing, although the disparities between
whites and African-Americans are likely to per-
sist. Those interracial disparities reflect social
problems, whereas the fact that women usually
live longer than men is likely to be genetically
determined.
Fig. 2-1 features the population pyramid, a
graphic method of showing age distribution, to
demonstrate some population dynamics in the
United States. The pyramid in Fig. 2-1, A, is from
the 1990 census14 and the pyramid in Fig. 2-1, B,
is from the 2000 census.15 The bulge of the
baby-boomer generation, the large number of
children born between 1946 and 1964 in the
aftermath of World War II (1939–45), is clearly
evident in the 25-39 age-groups in 1990 and
the 35-49 age-groups in 2000. Of interest to
dental practitioners is the aging of the popula-
tion and the predominance of women in the
oldest age-groups. As time goes by, the popula-
tion pyramid for the United States will come to
look more like a rectangle. Average age will con-
tinue to increase for the foreseeable future, and
an ever-increasing proportion of the population
will be in the older age-groups.
Fig. 2-1 illustrates two areas of important
population change. One is the growth in the

Age-group
85+
80-84
1990 75-79
70-74
65-69
60-64
55-59
50-54
45-49
40-44
35-39
30-34
25-29
20-24
15-19
10-14
5-9
4 and under
15 10 5 5 10 15
MALE FEMALE
A Population in millions
Fig. 2-1 Population pyramids for the United States, 1990 (A) and 2000 (B).14,15
middle years, the inexorable upward movement
of the baby-boomer bulge toward the older
years. Less obvious, and less publicized, is the
increase in the population 10-24 years old
between 1990 and 2000. These bars are notice-
ably longer in 2000 than in 1990, and the fact
that the numbers were not present in the birth
to 14 years groups in 1990 means that immigra-
tion is making its mark.
The Census Bureau estimates that the total
population of the United States in the year
2020, when many of today’s dental students
will be practicing, will be 325 million.16 The
rate of population increase during the 1980-95
period was generally around 0.9% per year,
which does not sound a lot but is still more
than 2 million people per year. To provide a
global perspective, the contrast between current
and projected population growth rates in some
high-income countries and low-income coun-
tries is shown in Fig. 2-2. The highest rates of
population growth are clearly occurring in the
low-income world. In the year 2000, the popu-
lation of the high-income countries was about
one-fifth of the world’s total.
Age Distribution
Low fertility rates since the late 1960s have com-
bined with increasing life expectancy to pro-
duce the “graying of America,” the term often
used to describe to the nation’s constantly
increasing average age. Those ages 65 years and
older were 11.2% of the population in 19796
2 The Public Served by Dentistry 15
Age-group
85+
80-84
2000 75-79
70-74
65-69
60-64
55-59
50-54
45-49
40-44
35-39
30-34
25-29
20-24
15-19
10-14
5-9
4 and under
15 10 5 5 10 15
MALE FEMALE
B Population in millions
and 12.6% in 2000,12 and are estimated to be
13.4% by 2010 and 18.5% by 2025 as the last of
the baby boomers approach 65 years.12 Fig. 2-3
shows the change in age distribution of the U.S.
population between 1980 and 2000, with
Census Bureau projections to the year 2020. The
main points to note are the continuing shrink-
age of the 29 years and under group as a propor-
tion of the total and the continuing growth in
the 65 years and older group. The elderly popu-
lation is not spread evenly around the country.
Although the proportion of persons aged 65
years and older in the United States was 12.6%
in 2000, it ranged from 18.1% in Florida to
5.1% in Alaska.
As noted, the U.S. population will continue
to get older in future years, with profound social
ramifications (e.g., for Social Security, housing,
medical care). This aging trend, already well rec-
ognized in dentistry by greater attention to geri-
atric dentistry, will clearly affect the types and
distribution of dental services in future years.
For example, population trends alone indicate
that there is likely to be a greater emphasis on
periodontic and maintenance care than on
treatment for children, even apart from trends
in the oral diseases (see Chapters 19-23).
Geographic Distribution
Extensive migration of people from one region
to another has long been a characteristic of the
United States. It still is, with 15% of the popula-
tion changing their address in 1998-99.13
16 Dentistry and the Community

Syria

3
Nigeria
Annual growth rate

Peru

Australia

United States
1
Norway

0
1950-60 1960-70 1970-80 1980-90 1990-2000 2000-10 2010-20

Growth period: years

Fig. 2-2 Rates of population growth, actual and projected, in six countries, 1950–60 to 2010–20.11

Percent Years Rhode Island grew by only 4.5% and that of

100 Pennsylvania by 3.4%.17 Since interregional
65+
migrants tend to be younger people, the median
80 age in the South, the mountains, and the West is
30-64
already lower than it is in the Northeast, and the
interregional differences are expected to remain
60
or even increase in the years ahead.
Reasons for the “Sun Belt” migration since
40
1970 are primarily economic. The nation’s eco-
<30 nomic base, once concentrated in the industries
20 of the Northeast and Midwest, has become
more spread out, and businesses in the com-
0 puter age have greater flexibility in choice of
1980 1990 2000 2010 2020 location than they used to have. The importance
Year of the Pacific Rim nations in the American
Fig. 2-3 Projected population distribution by age-group in
the United States, 1980–2020.7

A major trend since 1970 has been population 22.9% 19.0%

movement from the Northeastern, North 22.5%
Central, and Midwest regions to the South and
West, with the rate of population growth in
recent years being most pronounced in the 35.6%
mountain states. Fig. 2-4 shows the percentage
of total population by region for 2000. In the
decade of the 1990s, Nevada’s population
grew by 66%, Arizona’s by 40%, and Colorado’s Fig. 2-4 Population distribution by geographic regions in
by 30%. By comparison, the population of the United States, 2000.17

Percent
100 Asian-Pacific Islanders
Native American
Hispanic*
80
African-American
60
40
White non-Hispanic
20
0 large New York Hispanic population is predom-
2000 2010 2020 2030
Year
Fig. 2-5 Distribution of the U.S. population by race and eth-
nicity, 2000–30. (*In these data, Hispanics can be of any
race.)17
economy ensures that the West Coast will
remain a leading business area, as well as a stop-
ping place for immigrants from Asia. However,
some potential constraints to this pattern of
growth could change things. The main one con-
cerns access to limited water supplies, already a
major political issue in California. If the rapidly
growing cities in the region also develop the
social problems of the older northern cities,
they could become less attractive places to live.
At a different level, big cities continue to lose
population to suburbs and small towns and
are financially troubled as job opportunities
move out. The provision of dental services in
these inner city areas is one of many functions
that are adversely affected by these population
movements.
Racial and Ethnic Composition
The 2000 census of the United States listed 35.3
million African-Americans, which is 12.8% of
the total population. Persons of Hispanic
descent numbered 32.4 million, 11.8% of the
total, and the number is increasing rapidly.17
Because the racial and ethnic groups now
considered “minorities” are growing rapidly,
the term minority groups will lose much of its
current meaning during the twenty-first century.
Fig. 2-5 shows the percentages of various racial
and ethnic groups in the United States in 2000
and compares that distribution with the pro-
jected distribution over the next three decades.
The main features of Fig. 2-5 are the expansion
2 The Public Served by Dentistry 17
of the Asian–Pacific Islander population from
4% to 7%, the growth in the Hispanic popula-
tion from 12% to 19%, and the decrease in the
proportion of non-Hispanic whites from 71%
to 60% of all Americans.
By 2003 Hispanics had become the largest
minority group in the United States. Hispanic is
a generic term for Spanish-speaking persons
and covers a variety of cultures and even races.
Most of the Hispanic population is of Mexican
heritage, and many live in the Southwest. The
inantly Puerto Rican, and Cubans are centered
in Miami. One third of the Hispanic population
in the 2000 census was from other countries in
South or Central America or the Caribbean.17
Economic Distribution
The federal definition of poverty changes with
inflation and in 2003 was set as an annual
income of $18,400 for a nonfarm four-person
family in the contiguous United States. It is
higher in Alaska and Hawaii.18
A disturbing trend that became evident dur-
ing the 1980s, and has continued into the new
century, is the increase in the proportion of
Americans living in poverty. The proportion
of Americans in poverty through the 1980s was
13%-15%.8 There was some improvement dur-
ing the 1990s, but by 2002 the poverty rate was
12.1%, up from 11.7% in 2001.9 The problem
of poverty is especially pronounced among
America’s children and minority populations.
The proportion of the nation’s children ages
5-17 years living in poverty was 16.7% in 2002,
higher than the overall rate. Poverty is also
far more pronounced in minority groups: 8%
of the non-Hispanic white population, 24% of
African-Americans, and 22% of Hispanics were
in poverty in 2002.9
This heavy burden of poverty has implica-
tions for the provision of dental care, because
the problem of untreated oral disease is consid-
erably greater among people of low income and
education. This issue will be touched on fre-
quently throughout the book.
Summary of Population Trends
The American population is aging, and the
so-called minority groups comprise an ever-
growing proportion of it. The polarization
between richer and poorer segments is showing
18 Dentistry and the Community
no signs of ending, and the population contin-
ues to shift south and west. Some implications
for dentistry are that patients in their eighties
and nineties, and even some over 100 years of
age, will become common in dental practice,
and all dental personnel will need training in
the special needs of the older patient. The den-
tal professions will need to face the problems of
providing care for the 35 million people in
poverty, because the lack of access to dental care
among these groups is already a major public
health problem and will only grow further in
the absence of programmatic action. Adequate
provision of dental care for the growing minor-
ity populations may require more dentists from
those groups, and all dental professionals will
need to be culturally competent if they are to be
both effective and comfortable working with
minorities. These adaptations will all be basic
necessities if dental care for minorities is ever to
achieve the status in their lives that it has in the
lives of the majority.
UTILIZATION OF DENTAL SERVICES
The need for dental care can be defined as that
quantity of dental treatment that expert opin-
ion judges ought to be consumed over a certain
period for people to achieve the status of being
dentally healthy.4 This professionally deter-
mined dental need is sometimes called norma-
tive need. Need for an individual or population
can be expressed as (1) individual items of care
required, such as those entered on a patient’s
chart; (2) total professional time needed for
treatment; (3) the numbers of professionals
needed for a particular time; or (4) the total cost
of such care. Perceived need, also referred to as
subjective or felt need, is need for dental care as
determined by a patient or the public. Perceived
need can often differ considerably from norma-
tive need. For example, a dentist might judge
that a patient needs a root canal treatment fol-
lowed by a crown whereas the patient wants the
tooth extracted. Demand for dental care is the
expression by a patient or the public of a desire
to receive dental care to attend to their per-
ceived needs.3 Related terms are potential or
latent demand, meaning a desire for care that is
not being met for some reason.
Utilization is the actual attendance by mem-
bers of the public at dental treatment facilities
to receive dental care. Utilization is expressed as
(1) the proportion of a population who visited
a dentist within a given time, usually a year, or
(2) the average number of visits per person
made during a year. The latter measure gener-
ally uses the whole population as denominator,
so it is weighted by people who did not visit the
dentist at all over the time in question.
Annual Dental Attendance
Information on the use of dental services, in
addition to a lot of other health-related infor-
mation, comes from the continuing series
of household interviews conducted by the
National Center for Health Statistics, an agency
within the U.S. Department of Health and
Human Services. In 2001, 65.6% of people in
the United States reported that they had visited
a dentist within the previous year, the highest
proportion ever to do so.19 By way of contrast
with utilization some 30 years earlier, only 37%
reported visiting a dentist within the previous
year in 1957-58.22
Utilization of dental services in the United
States, as measured by those who reported mak-
ing at least one dental visit over the previous
year, rose modestly during the 1960s, plateaued
at about 50% during the 1970s, and then rose
noticeably during the 1980s. The upward trend
continues. At all times, more women than men
reported visiting the dentist. The trend of
increasing annual utilization over recent years,
for both men and women, is shown in Fig. 2-6.
FACTORS ASSOCIATED WITH THE USE
OF DENTAL SERVICES
The profile of the most frequent user of dental
services is a white, female, college-educated sub-
urbanite in a higher income bracket, who
enjoys good general health and has dental
insurance. The profile of the chronic nonuser is
a minority male, poorly educated, with little
money and certainly no dental insurance. The
variations in dental service utilization by demo-
graphic and other variables provide some basis
for predicting how dental services may be used
in the future.
Gender
As seen in Fig. 2-6, women report using dental
services more than men do. This finding is so

Percent
80
Female
70 Male
60
50
40
30
20
10
0
1958 1969 1973 1977
Fig. 2-6 Proportion of the U.S. population who reported having visited a dentist within the previous
year, by gender, 1958–2000.20,22–25
consistent over time, and so constant in all
countries that have studied the issue,1 that it
seems virtually universal—one of the few trends
of which we can say it “always” happens. No
one really knows why; numerous attempts to
explore the issue have not come up with con-
vincing explanations. In the past, vanity has
been suggested as a reason, but are women
really more vain than men? Unspecified “cul-
tural factors” is another suggestion, but the
trend is seen across a wide variety of cultures. It
has also been hypothesized that the largely
male composition of the dental profession is
part of the answer, but that proposition breaks
down with evidence from countries such as
Finland, where dental professionals are pre-
dominantly female.5 Women also make more
physician contacts than do men,21 so perhaps it
is just in the nature of things.
Age
The peak ages for dental visits have traditionally
been school age and the late teenage years, with
a gradual tailing off with increasing age. Service
2 The Public Served by Dentistry 19
1980 1983 1986 1989 1997 2000
Year
use has traditionally been low in preschool
years, and although it is improving, more than
50% of children aged 2-4 years had still never
visited a dentist in 1999.26 The distribution of
dental service use is also the polar opposite of
that for physician services, because use of physi-
cian services is highest among the youngest and
the oldest age-groups, in which use of dental
services is the lowest. The utilization curve
for medical care services has traditionally been
U-shaped, although as Fig. 2-7 shows it is
approaching a straight line. The dental services
utilization curve is still an inverted U shape. The
contrast between use of medical and dental
services is particularly important for adminis-
tration of managed care plans (see Chapter 7).
The traditional tailing off of dental service
use with increasing age is changing quite rap-
idly, however, as tooth retention among older
adults increases. Fig. 2-8 shows utilization by
age in 1969 compared with that in 1989; the
marked increase in the oldest and youngest age-
groups is obvious. As Fig. 2-6 shows, overall uti-
lization has increased even further since 1989.
20 Dentistry and the Community

Percent Percent
100 80

80
60

60
40
40

20
20

0 0
<5 5-17 18-44 45-64 65-74 75+ 35-44 45-54 55-64 65-74 75+

Dental Age-group Age-group

Dentate
Medical
Edentulous
Fig. 2-7 Contrasting patterns in the proportion of the U.S.
population using medical and dental services, by age, Fig. 2-9 Utilization of dental services by dentate and eden-
1999.26,27 tulous persons in the United States, 1989.25

Percent
tate people, there was little decrease in use of
80
dental services with increasing age.2 That analy-
70
sis showed that 59.5% of dentate persons ages
65-74 years reported a dental visit within the
60 previous year, which was actually more than the
58.4% utilization among dentate persons ages
50 25-34 years. Among edentulous persons of all
ages, however, annual utilization was only
40 12.6%. The distribution of annual dental visits
for American adults ages 35 years or older in the
30
1989 National Health Interview Survey, by age
and dentate-edentulous status, is shown in
20
Fig. 2-9. When the data are viewed in this way, it
10 is remarkable how uniform dental utilization
remains with increasing age when people retain
0 their teeth.
<5 5-17 18-24 25-44 45-64 65+
Socioeconomic Status
1969 Age-group
Socioeconomic status (SES) in the United States
1989
is usually measured by years of education and
Fig. 2-8 Increases in the utilization of dental services in the annual income, which not surprisingly are
United States, 1969–89.23,25
closely correlated. SES is directly related to use
of dental services: the higher the SES, the greater
Low use of dental services by older adults was the use of dental services. As with gender differ-
once thought to be caused by loss of interest in ences, this relationship is found consistently in
dental health with age, but in fact is more all countries, even in those where the cost bar-
related to loss of teeth than loss of interest. The rier for dental care has been reduced by public
difference was first pointed out in an analysis of financing. This pattern is illustrated by data for
1983 data from the National Health Interview the United States from 1989 presented in
Survey, in which it was found that among den- Fig. 2-10, which shows utilization for adults 22

80
60
Percent
40
20
0
22-34 35-44
13+ Years 9-11 Years
12 Years <9 Years
Fig. 2-10 Utilization of dental services by U.S. adults, by years of education received, 1999.26,27
years or older, by age, for four different educa-
tional levels. The close association between use
of dental services and educational levels is obvi-
ous, and the difference in the older age-groups
is especially marked. The majority of edentu-
lous people, and those without dental insur-
ance, are in the lower educational attainment
groups, so those factors would influence the
data seen in Fig. 2-10. Once again, it is remark-
able how uniform is the use of dental services
with increasing age among college-
educated people (13+ years of education).
Persons with higher incomes also visit the den-
tist more frequently than do persons with lower
incomes, and as noted earlier, income and edu-
cational level are tightly correlated in the
United States.
The pattern in 1999 was the same: dental visits
within the previous year were reported by 38.2%
of those with less than a high school diploma
and by 80.2% of those with a college degree.27
The reasons for this consistent relationship
between SES and use of dental services are more
complicated than they might appear. It is easy
to say that people of lower SES are less inter-
ested in oral health or less aware of the value of
dental care, but that often-heard assertion is
oversimplified. Values, attitudes, and expecta-
tions naturally vary among people with differ-
2 The Public Served by Dentistry 21
45-54 55-64 65+
Age-group
ent income and educational levels. Many lesser-
educated people are from backgrounds in
which dental care was virtually nonexistent, so
they have none of the middle-class culture of
which dental care is a part. More obviously,
lower SES groups are less able to afford care
when it does exist, and they are less likely to
have dental insurance. There are fewer dentists
in lower SES areas (see Chapter 8), so dental
care is less available; people just adapt to living
without dental care. Dental insurance has made
some difference to the problem of affording
care, but experience in a number of countries
has long shown that even when the cost barrier
is completely removed, clear disparities are still
seen in use of dental services among the differ-
ent socioeconomic groups.
Race and Ethnicity
In 2000 70.2% of white non-Hispanic Americans
reported visiting a dentist, compared with
57.5% of non-Hispanic African-Americans and
51.4% of Hispanic Americans.27 As noted ear-
lier, utilization data are not easy to interpret
because race and ethnicity in the United States
are inextricably related to wealth and poverty,
education, cultural values, and residential
location. Hispanics and African-Americans
have also suffered historically from deliberate
22 Dentistry and the Community
65.5% 68.2%
63.1%
58.3%
United States = 63.0%
Fig. 2-11 Proportion of the U.S. adult population reporting
a dental visit within the previous year, by geographic region,
1999.27
exclusion from many care facilities, and there
are relatively few dental providers from these
groups. The National Health Interview Survey
data for 2000 also show that 54.6% of Native
Americans and Alaskan natives reported a den-
tal visit, as did 66.3% of Asians.27 As noted ear-
lier, race and ethnicity are inextricably bound
into SES, geographic location, and availability
of dental care, so the disparity between whites
and minorities in dental visits again reflects all
of these factors.
Geographic Location
There are variations in frequency of dental visits
by region of the country, as shown in Fig. 2-11.
The Northeast, Midwest, and West show similar
usage patterns, but the South has a lower level
of utilization. The South has the lowest SES
ranking of the four regions, as well as the most
unfavorable dentist/population ratio, which
probably are major factors in explaining these
variations.
General Health
People who consider themselves in excellent
health visit a dentist more often than those who
see themselves as in good or only fair health.
Among those who considered themselves to be
in “excellent” health, 61.9% reported a visit dur-
ing 1989 compared with 51.5% who thought
their health was “good” and 39.8% who thought
it was “fair or poor.”25 Distributions of a similar
nature were found among those who had no
restriction of activity compared with those
whose activity was limited to some degree.
These findings are hardly unexpected,
because people whose mobility is restricted
quite naturally would find getting to a dentist
more difficult. Those in poor general health
may be too preoccupied, or too restricted gener-
ally, to face going to the dentist. These distribu-
tions also are likely to be related to age and to
SES.
Dental Insurance
People with dental insurance visit a dentist
more often than do people without insurance.
The 1999 data showed that 71.9% of adults
aged 18–64 years with private dental insurance
visited a dentist within the previous year, com-
pared with only 38% of those without.27 The
contrast for all age-groups, using 1989 data, is
shown in Fig. 2-12.
These differences are to be expected because
dental insurance can substantially reduce the
financial burden of dental care. It was men-
tioned earlier that cost is not as much of a bar-
rier to receiving dental care as is often thought.
Even among groups for whom there is no direct
charge for dental treatment, the association
between utilization of care and SES is still seen.
To explain the role of dental insurance, we must
look at who has it: professionals, white-collar
workers, and members of the larger labor
unions who receive group dental care as a fringe
benefit of employment. So again, there is likely
to be an association with SES as well as some
financial incentive for these groups.
FUTURE USE OF DENTAL SERVICES
Should we expect the trend of steadily increas-
ing dental utilization to continue? If so, how far
before it hits a ceiling? These questions are of
fundamental importance to students and new
graduates, and the data presented give us a basis
for making estimates.
Apart from gender, the data show that the
most powerful correlates of dental utilization
are SES, dentate status, and the extent of dental
insurance. Overall economic conditions are
also a major factor. Prosperity provides more
disposable income for people to afford dental
care, permits employers to offer more generous
dental insurance plans, and leads to a feeling
of optimism. If economic conditions in the
United States decline over the long term, how-

Percent
100
80
60
40
20
0
<11 12-17
With insurance
Without insurance
Fig. 2-12 Proportion of U.S. adults reporting a dental visit within the previous year, by age and status of dental
insurance, 1989.25
ever, more people will be forced out of the mid-
dle classes and use of dental services will
decline. Poor economic conditions would force
many corporations to drop dental insurance,
which would also reduce the use of dental
services.
Increasing tooth retention (see Chapter 7),
especially among the elderly, is reason for opti-
mism about an increase in the use of dental
services by the next generation of older
Americans. The data clearly show that when
people are dentate, they go to the dentist; when
they are edentulous, they do not.
As stated earlier, population growth in the
United States in recent years has been greatest
in the lower SES groups, among African-
Americans and Hispanics, groups with rela-
tively low use of dental services. Immigration is
a major force in population growth, and many
of the new immigrants from the Spanish-
speaking world live in deep poverty. Because
these groups make up a larger proportion of the
population (see Fig. 2-5), rigid adherence to
current methods of providing dental care will
lead to a decline in utilization. People in these
social strata are largely outside the usual dental
insurance groups, and the cuts in public health
programs through the 1980s left many of them
with little opportunity to receive dental care at
all, let alone to adopt habits of regular atten-
dance. Growth in the population utilizing den-
tal services will require the introduction of the
2 The Public Served by Dentistry 23
18-34 35-44 45-54 55-64 65+
Age-group
lower SES population to dental care, which in
turn will require more resources in the public
health sector to provide the necessary education
and acculturation.
SUMMARY
The use of dental services is tied closely to eco-
nomic developments and demography, neither
of which dental personnel can do much to
influence. Increasing tooth retention is one fac-
tor that tends to increase utilization among
older Americans. The utilization patterns of
younger generations are harder to predict, and
overall utilization could remain at current lev-
els, but with a distributional shift away from
younger toward older patients. Specific pro-
grams aimed at bringing today’s minority
groups into the dental care system will also be a
major step toward improvement of the nation’s
oral health. Without such action, utilization
of dental services could go into long-term
decline.
REFERENCES
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 3 Ethics and Responsibility in Dental
Care
FRAMEWORK FOR ETHICAL
STANDARDS
INDIVIDUAL VERSUS SOCIAL
RESPONSIBILITY
INDIVIDUALISM IN THE UNITED STATES
RIGHT TO HEALTH CARE
As noted in Chapter 1, professionalism brings
with it the responsibility to adhere to the high-
est ethical standards. Public trust is the greatest
asset that the dental professions possess, and
that trust has been hard-earned by the profes-
sions’ willingness to adhere to ethical practice
and to follow through if there has been a
breach. Even the most conscientious practi-
tioner will find that ethical dilemmas arise fre-
quently. For example, how does a practitioner
respond to a patient who wants all her amalgam
restorations removed because she believes they
are the cause of her chronic fatigue? What is the
practitioner’s obligation in treating a patient
who is mentally unable to provide his own
informed consent? Straight answers are not
always easy to find, although ethical codes are
intended to give the practitioner guidelines to
follow.
This chapter discusses the place of profes-
sional ethics in dental care. We discuss the
framework for ethical codes, the social and cul-
tural background against which our ethical
standards have evolved, ethics in patient care
and research, and the role of the professional
associations in defining ethical codes.
FRAMEWORK FOR ETHICAL
STANDARDS
Ethics, a branch of philosophy and theology, is
the systematic study of what is right and good
with respect to conduct and character.27 Ethics
PROFESSIONAL ETHICS AND SELF-
REGULATION
Ethics in Patient Care
Ethics in Research
DENTISTRY’S ETHICAL CHALLENGE: ACCESS
TO CARE FOR EVERYONE
has also been used as a generic term for various
ways of understanding and examining the moral
life.8 Our understanding of ethics can also be
helped by defining some things that ethics is not:
it is not a set of rules or restrictions, it is not reli-
gion, and it is neither relative nor subjective.24
The very nature of moral decisions means
that much of the ethics literature asks questions
rather than provides answers, and this lack of a
“formula” to solve problems can be frustrating
for some. Because ethics is the study of both the
general nature of morals and of specific moral
choices, ethical decisions can vary over time and
between locations when cultural standards dif-
fer. This means, as noted earlier, that a formula
for finding what is the right thing to do in spe-
cific circumstances cannot always be provided,
only guidelines.
The dictum “First, do no harm” has been
around since Hippocrates, around 400 BC, and
from that point ethical principles have devel-
oped slowly over the centuries. Today there are
four basic principles (Box 3-1) that have
become widely accepted as guidelines for deci-
sion making in biomedical ethical dilemmas
and that apply to dental professionals as they
do to physicians and nurses.
For a professional organization, these princi-
ples then need to be formulated as ethical stan-
dards. Standards can take the following forms:
●
Aspirational, a broadly worded statement of
ideals. No precise definitions of right or
wrong behavior are given.
25
26 Dentistry and the Community
BOX 3-1 Summary of Ethical Guidelines for Biomedical Decision Making8
Educational, which combine the principles
●
with explicit guidelines that can assist
decision making in morally ambiguous
situations.
Regulatory, which go a step further and
●
include a set of detailed rules to govern pro-
fessional conduct and which serve as a
basis for adjudicating grievances. Such
rules are assumed to be enforceable, with a
range of sanctions imposed by the profes-
sion if the rules are contravened.14
Professions adopt ethical standards because
that is part of the professional charge. A
patient’s trust in a professional comes in part
from the expectation that the professional’s
behavior is governed by norms prescribed by
the group.14 It is also a public expectation that
ethical standards be developed and enforced by
any profession, a requirement that comes with
the privilege of self-regulation.
It was stated earlier that ethical standards are
shaped in part by cultural forces, so it is well to
examine briefly some of the social and cultural
forces that underlie ethical expectations in the
United States.
INDIVIDUAL VERSUS SOCIAL
RESPONSIBILITY
Who is responsible for health? Is it society as a
whole, or is health each individual’s responsi-
bility? That is a broad question, to which the
answer can only be, “Some of both.”
It is well understood today that individual
lifestyle choices are a major factor in determin-
ing a person’s health status. Every educated per-
son knows the basic rules: don’t smoke, drink in
moderation, eat lots of fresh fruit and vegeta-
bles and a varied diet low in saturated fats, get
enough sleep, exercise regularly, fasten the car’s
seatbelt, maintain friendships and social con-
tacts. But what about those individuals who are
unfortunate enough to have genetic predisposi-
tions to disease or are mentally or physically
handicapped? Or those who live in rundown
neighborhoods where food choices are limited
and there is little opportunity to practice a
healthy lifestyle? Many people became addicted
to cigarettes at a time when such addiction was
not understood, and some became alcoholic or
drug-addicted in response to social or personal
pressures. The problems these conditions pres-
ent can be compounded by the individual’s
inability to pay for necessary medical care. What
are the professions’ ethical obligations in these
and related instances?
If we believed that health is solely an individ-
ual responsibility, we would shrug our shoulders,
say “Bad luck,” and be thankful that these bad
things weren’t happening to us. But we don’t do
that. All high-income nations accept some
degree of public responsibility through health
and social support systems for sick people. In
many European countries, Canada, Australia,
and New Zealand these systems can be extensive,
usually more so than their counterparts in the
United States. Arguments in the United States
can turn toward whether such programs should
exist at all, although most balk at suggestions
that the last vestiges of a “safety net” should be
removed. There is ongoing vigorous debate,
however, about the extent of and eligibility crite-
ria for public financing of health and welfare,
and about the right division between public and
personal financing for them. American attitudes
toward publicly financed social systems are gen-
erally not as positive as those in other developed
countries, so it is worth looking at how American
cultural attitudes toward individualism and
social responsibility have evolved.

INDIVIDUALISM IN THE UNITED
STATES
Americans rightly cherish their individual rights
and freedoms; individualism has been a more
powerful cultural force in the United States than
in other countries.9 Many of the settlers who first
immigrated to America (voluntary settlers at
least) were leaving rigid social, religious, or politi-
cal systems to seek a new life where they and their
children could prosper in an environment that
was free of the constraints they had left behind,
and where hard work would create its own oppor-
tunities and yield its own rewards. An abundance
of natural resources and a seemingly limitless
frontier gave rise to the attitude that in America
people could mold their own destinies largely by
their own efforts. Although historical evidence
shows that this belief is at best only partly true,9 it
still remains a powerful cultural perception and is
still the magnet attracting today’s immigrants.
The high point of unfettered laissez-faire cap-
italism occurred in western Europe around the
mid-nineteenth century and in the United States
a generation or so later. By the early years of the
twentieth century, however, philosophies in
Europe were turning away from individualism
toward more shared responsibility for basics like
housing, education, social security, and health
care. Programs grew slowly, but by the 1970s, a
network of national state-sponsored social pro-
grams was the norm in Europe, less so in the
United States. Why the more hesitant growth in
America? One reason suggested for the slower
development in the United States is that
America’s relative isolation from external politi-
cal turbulence during its formative years allowed
the development of a more introspective
national character than was the case in Europe.28
Another reason, given that catastrophic events
have a way of hastening social change, is that the
social devastation wrought by two major wars in
the first half of the twentieth century hastened
the development of social welfare programs in
Europe. The United States largely escaped the
social devastation of those wars. It should be
remembered, however, that the first Social
Security Act in the United States was passed in
1935 in the midst of the Great Depression,
which was a catastrophe by any measure.
Another major contribution to the individu-
alist culture in America comes from what is
3 Ethics and Responsibility in Dental Care 27
referred to as the puritan ethic, which historians
consider to have arrived with the first English
colonists.11 Many of these and other pioneers
were members of nonconformist religious
groups who brought their rigid beliefs about
human nature to the new land. These attitudes
became part of the American national character,
and as such they remain prominent today.
Essentially, the puritan ethic is a set of beliefs
and attitudes which holds that God rewards
people for their honest toil in this life as well as
in the next, and that individual wealth or
poverty is justified and largely controllable by
one’s own efforts. It follows that under the puri-
tan ethic the accumulation of great personal
wealth can be seen as a reward for virtue and
hard work, just as poverty can be seen as a pun-
ishment for immorality or laziness. It logically
follows that the puritan ethic also involves a
strong aversion to paying taxes, especially when
the funds can be “wasted” for social programs
aimed at helping the “undeserving” poor.
The first serious questioning of individualism
in the United States came during the widespread
social distress caused by the Great Depression of
the 1930s. Many people at that time lost every-
thing through what was clearly no fault of their
own, and the response of the federal government
was a series of emergency relief measures aimed
at avoiding total societal collapse. Most of these
no longer exist, although Social Security has not
only survived but has become institutionalized
as a major entitlement that figures prominently
in current political debate. World War II
(1939–45) followed the depression, after which
the next wave of social activity followed the reve-
lations about the extent and consequences of
poverty in the United States during the early
1960s. The Eighty-ninth Congress (1964–65)
passed a series of legislative measures intended
to improve social equity, the main ones being the
Medicare and Medicaid health programs (see
Chapter 8), the Voting Rights Act, the Economic
Opportunity Act, the Model Cities Act, and
the Elementary and Secondary Education Act.
This trend was slowed, and in some cases
reversed, by the more conservative mood that set
in during the 1980s and continues today. This
public mood was also affected by a growing
awareness of limited resources and a loss of faith
in government’s ability to solve complex social
problems.
28 Dentistry and the Community
RIGHT TO HEALTH CARE
American attitudes, historically shaped by indi-
vidualism and the puritan ethic, are evolving
only slowly to the belief that access to health
care is a right rather than a privilege.7 The “right
to health care” is an emotional and often mis-
understood concept, one frequently interpreted
as “the right to health.” Of course, no one has a
right to health. Health, an elusive entity to
define, is a dynamic state influenced by genetic
endowment, nutrition, housing, physical and
social environment, life habits, personal atti-
tudes and beliefs, and medical care received,
quite possibly in that order of importance.
Although medical care has probably been over-
valued as a determinant of health,7,16,18 most
individuals at some time in their lives have a
need for it, sometimes an urgent need.
Health care has always been rationed in one
way or another. The traditional rationing
method has been fee for service, meaning that
those who can afford care get it, whereas those
who cannot afford it do not. The method is sim-
ple enough, and it conforms with the puritan
ethic, although there is an untold cost in wasted
human resources. This philosophy was chal-
lenged in the United States during the 1960s,
when access to health care was extended to mil-
lions of poorer citizens through Medicaid and
to the elderly through Medicare (see Chapter 7).
As would be expected, one result of better access
to care was that public expenditures on medical
care increased substantially. When the public
mood later swung toward controlling medical
care expenditures as the first priority, “managed
care” emerged in the 1980s and grew rapidly in
the 1990s (see Chapter 7). Managed care
appeared to reduce the rate of increase of med-
ical expenditures, although it did so by intro-
ducing other forms of rationing (e.g., restricting
services and which physicians may be con-
sulted). The ethical problems have multiplied
as a result.
PROFESSIONAL ETHICS AND
SELF-REGULATION
The American Dental Association (ADA) main-
tains a code of ethics, which is reviewed and
amended periodically by the association’s
Council on Ethics, Bylaws, and Judicial Affairs.
The current version of the code of ethics can be
found on the ADA’s website.4 It has three sec-
tions: Principles of Ethics, Code of Professional
Conduct, and Advisory Opinions. This code is
classified as aspirational by the ADA, meaning
that it is made up of broad principles, though
parts of it seem to be more educational, as
defined by the standards listed earlier. It is pri-
marily concerned with issues related to the care
of patients, though it also deals with the han-
dling of fees, referrals, criticism of colleagues,
advertising, and specialty practice. The code has
been modified over the years as new issues arise
and as societal views on particular issues
evolve. It is also influenced by judicial out-
comes, which presumably represent social val-
ues, as evidenced by growth in the legal
advisory opinions in the code. As an example,
the 1982 statement on patient selection stated
the following:
While dentists, in serving the public, may exercise rea-
sonable discretion in selecting patients for their practices,
dentists shall not refuse to accept patients into their prac-
tice or deny dental service to patients because of the
patient’s race, creed, color, sex or national origin.2
That statement was unchanged in later versions
of the code, but there was an advisory opinion
appended after 1988 that dealt primarily with
treating infected patients. This opinion stated
the following:
A dentist has the general obligation to provide care to
those in need. A decision not to provide treatment to an
individual because the individual has AIDS or is HIV
seropositive, based solely on that fact, is unethical.
Decisions with regard to the type of dental treatment
provided or referrals made or suggested, in such
instances, should be made on the same basis as they are
made with other patients, that is, whether the individ-
ual dentist believes he or she has need of another’s skills,
knowledge, equipment or experience and whether the
dentist believes, after consultation with the patient’s
physician if appropriate, the patient’s health status
would be significantly compromised by the provision of
dental treatment.3
This advisory opinion, maintained in the 2003
version of the code, is an example of an issue
that causes misgivings among some practition-
ers who do not feel it unethical to turn away a
patient who has tested positive for human
immunodeficiency virus on the grounds that
the health of the dentist and staff would be

unduly at risk if treatment were offered. (Note:
not only is such behavior unethical, it is also
illegal.12) By the new century, this issue had
advanced to the point where the code in Section
2.E stated the following:
All dentists, regardless of their bloodborne pathogen
status, have an ethical obligation to immediately inform
any patient who may have been exposed to blood or
other potentially infectious material in the dental office
of the need for post exposure evaluation and follow-up
and to immediately refer the patient to a qualified
health care practitioner who can provide postexposure
services.4
Another area in which professional viewpoints
have changed is in reporting bad treatment by
other dentists. Not very long ago those in the
biomedical professions considered it unethical
to report poor treatment by a colleague that
they observed. The response to seeing substan-
dard care was very much to close ranks. By the
new century, this had turned around, so that
Section 4.C reads:
Dentists shall be obliged to report to the appropriate
reviewing agency as determined by the local component
or constituent society instances of gross or continual
faulty treatment by other dentists. Patients should be
informed of their present oral health status without dis-
paraging comment about prior services. Dentists issuing
a public statement with respect to the profession shall
have a reasonable basis to believe that the comments
made are true.4
Not all aspects of practice are covered by the
ADA code of ethics. For example, the obligation
to keep current through continuing education
and reading the literature, a prime ethical
responsibility,22 is nonetheless given only cur-
sory mention in the ADA code. Although some
think that this issue could be stated more
strongly, perhaps it is being overtaken by events.
Minnesota was the first state to introduce
mandatory continuing education as a require-
ment for dental relicensure in 1969, and by the
mid-1990s almost every state had such a
requirement in place. It could be argued that
continuing education is therefore no longer an
ethical responsibility but a legal one. It would
be a pity, however, if continuing education
came to be interpreted solely as a legal require-
ment, for uncaring practitioners can always
fulfill the requirements on paper without trans-
ferring the knowledge to practice. Regulations
3 Ethics and Responsibility in Dental Care 29
aside, the ethical responsibility still remains for
practitioners to do their best to keep themselves
current.
Community service is also dealt with rather
vaguely in the ADA code. Section 3.A of the
code states the following:
Since dentists have an obligation to use their skills,
knowledge, and experience for the improvement of the
dental health of the public and are encouraged to be lead-
ers in their community, dentists in such service shall con-
duct themselves in such a manner as to maintain or
elevate the esteem of the profession.4
Some dentists working for a fluoridation cam-
paign in the community, for example, have felt
that an appearance on local television may con-
travene the spirit of the ethical constraint on
false and misleading advertising, even if such an
appearance would help the campaign. This
unduly cautious interpretation has to be
respected, though the statement in the code was
never intended to preclude such obviously pub-
lic-spirited activity. Some would like to see
Section 3.A of the code strengthened to encour-
age dentists to work cooperatively with public
health authorities for the benefit of the whole
community.
Dental hygienists should all be familiar with
the code of ethics adopted by the American
Dental Hygienists’ Association (ADHA).5 Aspects
dealing with professional conduct and patient
care are generally similar to those in the ADA
code. The ADHA lists as “basic beliefs” that all
people should have access to health care and to
oral health care, and that people are responsible
for their own health and entitled to make
choices regarding their health. No such state-
ment about access to health care can be found
in the ADA code.
Dentists may not give much thought to the
ethical problems of hygienists, but a national
survey of ADHA members in the late 1980s dis-
closed that the three most frequent ethical
issues faced by hygienists were (1) observation
of a dentist’s behavior in conflict with standard
infection control procedures; (2) failure of the
dentist to refer patients to specialists, such as
periodontists; and (3) nondiagnosis of oral dis-
ease by the dentist.17 Although 86% of those
responding said that they had some instruction
in ethical theory, only 51% reported that they
had received instruction in how to cope with
30 Dentistry and the Community
these ethical problems. It is noted that the cur-
rent ADHA code of ethics includes a require-
ment in the section To the Community and
Society for a hygienist to report inappropriate,
inadequate, or substandard care to the proper
authorities. In the same section there is an item
that states, “Recognize and uphold our obliga-
tion to provide pro bono service.”5 In general,
the ADHA code mixes some assertive state-
ments about dental hygiene practice with a
stronger community outlook than is found in
the ADA code.
The social climate of recent times has led
many professional organizations to develop
their own codes of ethics. There are of course
some overlaps; ethical conduct for an ortho-
dontist is basically no different than that for a
periodontist. But these codes also address mat-
ters specific to the discipline. The code of
ethics of the American Public Health
Association, for example, provides a statement
of the key values and beliefs inherent to the
public health perspective on which the ethical
principles are based.6 The preamble goes on to
say:
The code is neither a new nor an exhaustive system of
health ethics. Rather, it highlights the ethical principles
that follow from the distinctive characteristics of public
health. A key belief worth highlighting, and which under-
lies several of the ethical principles, is the interdependence
of people. This interdependence is the essence of commu-
nity. Public health not only seeks the health of whole com-
munities but also recognizes that the health of individuals
is tied to their life in the community.6
The emphasis on community is a keystone of
public health (see Chapter 4) and is somewhat
BOX 3-2 Declaration of Geneva, Adopted in 1948 by the World Medical Association29
Physician’s oath, taken at the time of being admitted as
a member of the medical profession:
●
I solemnly pledge myself to consecrate my life to the
service of humanity.
●
I will give to my teachers the respect and gratitude
which is their due.
●
I will practice my profession with conscience and dignity;
the health of my patient will be my first consideration.
●
I will maintain by all the means in my power, the honor
and the noble traditions of the medical profession; my
colleagues will be my brothers.
at odds with the individualist tradition
described earlier. Likewise, the ethical code of
the American Association of Public Health
Dentistry emphasizes community action and
care.1
Ethics in Patient Care
The world was jolted by the atrocities, in the
name of medical experimentation, committed
by Nazi Germany on prisoners in concentration
camps during World War II. In a reaction
against these appalling crimes, the World
Medical Association, a group of national med-
ical associations rather like the FDI (see
Chapter 1), adopted the Declaration of Geneva
in 1948.29 The principles of the declaration are
in the form of a physician’s oath, to be taken at
the time of graduation, and the oath itself is
shown in Box 3-2. Written in idealistic terms in
a time of postwar optimism, its emphasis is on
the primacy of patient care, a natural response
to the horrors of the war.
Society’s bestowing of self-government upon
the dental profession comes from its recogni-
tion that the profession conducts itself in a fair
and honorable manner in its contacts with
patients. As discussed in Chapter 1, this is one
of the cornerstones of professionalism. The
ADA states that “the ADA Code is, in effect, a
written expression of the obligations arising
from the implied contract between the dental
profession and society.”4
Because the professional has knowledge
that the patient does not and is usually in a
position to evaluate likely treatment out-
comes better than the patient, the professional
carries the burden of avoiding paternalism
●
I will not permit considerations of religion, nationality,
race, party politics or social standing to intervene
between my duty and my patient.
●
I will maintain the utmost respect for human life from
the time of conception, even under threat, I will not use
my medical knowledge contrary to the laws of humanity.
●
I make these promises solemnly, freely and upon my
honor.

and sharing her knowledge and experience with
the patient in such a way that the patient can
make informed choices.22 Even with the best of
intentions this is frequently difficult to do, espe-
cially when a patient yearns to put unqualified
trust in the professional:
Although intellectually patients—including doctors
when they become patients—know that doctors are not
infallible, emotionally we want to believe that they are,
that they know what they are doing and are capable of
doing it. The most skeptical of us longs to leave such skep-
ticism in the waiting room.15
This situation can force the professional to
take a paternalistic role, no matter how reluc-
tantly, and it can sharpen the conflict between
professional and proprietary values that fre-
quently arises in dental practice.21 Some have
argued that dentistry needs well-defined stan-
dards of care to fall back on in such circum-
stances,15 but the profession has never been
comfortable about defining such standards
because of its reluctance to take action that
might be seen as infringing upon professional
judgment. The ADA took a hesitant step in the
direction of standards with its Dental Practice
Parameters, adopted by the House of Delegates
in 1994–95, in which the broad descriptions
of what constitutes acceptable procedures are
preceded by statements that the clinical judg-
ment of the dentist comes first. These parame-
ters might have added that dentists have the
obligation to form their clinical judgments
based on the best available science, rather than
a personal preference or unfounded belief,
which is the essence of “evidence-based den-
tistry” (see Chapter 12). Discharging this pro-
fessional obligation requires dentists to have a
good grasp of what constitutes scientific study
(see Chapter 13) and to keep up with the liter-
ature and with continuing education.
Regardless of what framework for studying
ethics is used, the requirement to maintain
professional competence is a prime ethical
responsibility.22
Ethics in Research
Researchers bear the responsibility for identify-
ing and propagating truth in matters of science.
Much research involves studies with humans
and human tissues, as well as with animals, and
there are strict rules governing research with
3 Ethics and Responsibility in Dental Care 31
both. As with patient care, the first detailed
research codes were developed in the shadow of
World War II. The revulsion that followed the
disclosure of Nazi “experiments” brought seri-
ous public scrutiny to patients’ rights in
research studies and resulted in the 1947
Nuremberg Code,20 which introduced the
requirements that research subjects be able to
exercise choice and have the legal and intellec-
tual capacity to give consent, and be able to
understand to what they are consenting.19 Over
the years since then, the Nuremberg Code has
served as the basis for the extensive legal
requirements that many countries have devel-
oped to govern the participation of humans in
research. In addition to drafting the Declaration
of Geneva (see Box 3-2), which was aimed at
patient care, the World Medical Association has
further refined the subject of the rights of
human participants in research through the
Declaration of Helsinki in 1964, its subsequent
amendments,30 and a host of national and pro-
fessional codes since then.
The Declaration of Helsinki uses forthright
language: “considerations related to the well-
being of the human subject should take prece-
dence over the interests of science and society.”
For example, with respect to the role of placebos
in clinical trials (see Chapter 13), the declara-
tion stated the following in 2000:
The benefits, risks, burdens and effectiveness of a new
method should be tested against those of the best current
prophylactic, diagnostic, and therapeutic methods. This
does not exclude the use of placebo, or no treatment, in
studies where no proven prophylactic, diagnostic or thera-
peutic method exists.30
This statement was expanded in the 2002
meeting of the World Medical Association
to say:
The WMA hereby reaffirms its position that extreme
care must be taken in making use of a placebo-controlled
trial and that in general this methodology should only be
used in the absence of existing proven therapy. However, a
placebo-controlled trial may be ethically acceptable, even
if proven therapy is available, under the following
circumstances:
●
Where for compelling and scientifically sound
methodological reasons its use is necessary to deter-
mine the efficacy or safety of a prophylactic, diagnos-
tic or therapeutic method; or
32 Dentistry and the Community
BOX 3-3 Statement of Principles Adopted by the International Association for Dental Research (IADR) to Be
Applied to Dental Research23
All members of the IADR shall
●
Act with honor and in accordance with the highest
standards of professional integrity.
●
Be guided by the conventions of scholarly pursuit.
●
Promote exemplary ethical standards for research and
scholarship.
●
Conduct work with objectivity.
●
Communicate information in a responsible manner,
with due regard for the significance and credibility of
the available data.
●
Present scientific or professional judgments with full
disclosure of the extent of factual support.
●
Where a prophylactic, diagnostic or therapeutic
method is being investigated for a minor condition
and the patients who receive placebo will not be sub-
ject to any additional risk of serious or irreversible
harm.30
Legal requirements aside, researchers always
have the ethical obligation to treat all human
research volunteers with respect and dignity.
Codes for treatment of animals in research are
also now well developed.
In the United States, formulation of codes of
ethics in research is now mostly based on
the Belmont Report.25 The National Research
Act of 1974 (Public Law 93-348) brought into
being the National Commission for the
Protection of Human Subjects of Biomedical
and Behavioral Research. The commission iden-
tified the basic ethical principles intended to
underlie the conduct of biomedical and behav-
ioral research involving human subjects, and it
developed guidelines to be followed to ensure
that such research is so conducted. The report is
a statement of basic ethical principles and
guidelines to assist in resolving the ethical prob-
lems that surround the conduct of research with
human subjects.
The International Association for Dental
Research (IADR) is the umbrella organization
for dental research activities around the world.
The IADR approached the ethical issue by
adopting a preamble and principles for a code
of ethics.23,24 Given the range of cultural val-
ues of those involved in research, the IADR
considered that trying to set a single ethical
●
Avoid judgments influenced by conflict of interest.
(Specifically, this refers to situations in which a researcher
stands to gain financially or professionally from a decision
in which he or she participates. Full disclosure of any
potential conflict of interest must be made.)
●
Take actions necessary to ensure the rights and
interests of research subjects, and observe the spirit
and letter of laws, regulations, and ethical standards
with regard to the welfare of humans and animals
involved in experimental or clinical procedures.
●
Not engage in any form of advertising that is false,
fraudulent, deceptive, or misleading.
code for the whole world would seem too
authoritarian and would lack local buy-in.
Instead, the intent is that its divisions (usually
individual countries or groups of countries)
will use the preamble and principles, plus
other parts of the comprehensive report on
ethics,23 to develop their own codes. Despite
periodic encouragement through the IADR
and periodic symposia on ethics in research at
IADR annual meetings, progress toward this
goal has been slow. The IADR’s statement of
research principles directed at its members,
shown in Box 3-3, is clearly aspirational in
nature. The principles applying specifically to
research with human subjects (Box 3-4),
included in the IADR’s report in 1994 but
never formally adopted, are more specifically
educational. Indeed, parts of these principles
have become regulatory in the United States
and other countries.
The trend in the United States is toward ever-
expanding regulations governing research with
human subjects, especially documentation of
informed consent. Every institution in which
research involving human subjects takes place is
required to have an institutional review board,
whose task it is to review all research proposals
before the research actually starts to ensure that
regulations for the protection of human sub-
jects have been followed. Punishment for not
complying with these regulations can be strict—
several major research universities have had all
research funding cut off until alleged human
subjects’ transgressions have been corrected.

BOX 3-4 Ethical Principles for Research Involving Human Subjects23
●
The research must be scientifically sound, with an
identifiable prospect of benefit.
●
Human subjects must be selected equitably.
●
Risks to humans, and the numbers of humans
involved, must both be minimized.
●
Voluntary informed consent must be obtained from all
human subjects, or from their proxies, before any
research is started.
●
Human research subjects must be permitted to
withdraw from the research at any time and to be
Although some researchers look on institu-
tional review board requirements as a burden, it
is better to look on them as just one of the basic
requirements of a complete research protocol.
It has been suggested that codes of research
ethics need to distinguish between two types of
problematic practices: those that are clearly mis-
conduct because they undermine the trustwor-
thiness of science (e.g., data falsification) and
those that are unethical but are better described
as disrespectful of the work of others. An exam-
ple of the latter kind is plagiarism, which is
unethical but rarely undermines the trustwor-
thiness of science.10 Plagiarism, which is cir-
cumventing attribution to represent the works
or ideas of others as one’s own, has always been
around, but the Internet is highlighting the
issue more than ever. Some who would never
lift a paragraph from a book or journal without
attribution have no such qualms about lifting
Internet material without attribution, even
though the principles are the same.
DENTISTRY’S ETHICAL CHALLENGE:
ACCESS TO CARE FOR EVERYONE
An overriding ethical challenge to the dental
professions is to meet their stated aims of bring-
ing oral health care to all members of the pub-
lic. This commendable goal can only be reached
with the right mix of public and private care.
The vast majority of the dentist-attending
public receives its dental care from private prac-
titioners. Private practice in the United States is
well suited to the healthy, employed, dentally
conscious, compliant, middle-class patient for
whom accessibility to private care is rarely a
3 Ethics and Responsibility in Dental Care 33
assured that such withdrawal will not prejudice any
ordinary treatment, if they are receiving any.
●
Human subjects must be removed from the research
project as soon as there is any indication of possible
harm, whether physical or psychological, being done to
them as a consequence of their being research subjects.
●
The privacy of human subjects and the confidentiality
of the data about them must be protected.
●
Research results must be written honestly and
accurately.
problem and who can generally afford neces-
sary treatment (frequently assisted by insur-
ance). Private practice has adapted readily
to dental insurance since that payment
mechanism began to grow in the 1960s, and
this serves to make private practice even more
attractive. The oft-used expression “the best
dental care in the world” is accurate enough in
these circumstances.
Not every prospective dental patient in the
United States, however, fits the category just
described. As discussed in Chapter 2, some
12% of Americans exist below the federal
poverty line, and millions of others live on the
fringe of poverty. It is a major challenge for the
nation to find ways of making health care
accessible to the steady proportion of
Americans without health insurance of any
kind. This proportion has been around 16%-
17% of the population for years, and despite all
the hand wringing that goes on it is not getting
any lower.26 (This figure is for general health
insurance, not dental insurance. The propor-
tion without dental insurance is around 40%.)
Intertwined with the world of poverty are the
homeless, the unemployed and unemployable,
and the homebound and chronically ill. The
marginally mentally retarded, who used to
reside in institutions, can have the capacity and
the will to work but need social supports to do
so. When these are not available, these individ-
uals can drift off into dependency again. For
those who remain institutionalized for mental
and physical disabilities, dental care is sporadi-
cally available at best. Then there is a virtual
army of working poor, usually uninsured and
in minimum-wage positions, who can find the
34 Dentistry and the Community
typical private practice not only expensive but
also intimidating.
It is really a cultural matter, for these are
groups for whom regular visits to the dentist
occupy no place in their lives. Not only is such
care financially out of reach for the people con-
cerned, but also many practitioners can signal
the message, often inadvertently, that they
would prefer not to have to treat such patients.
Private practice is most efficient when patients
understand the need for care, know how to
behave while receiving treatment, and are from
the same socioeconomic level as the dentist. But
handicapped people take longer to treat and
often require special equipment and training to
be treated satisfactorily, and the circumstances
of poverty mean that the poor are often inter-
ested only in minimal care and frequently skip
appointments. As a consequence, dental care
for many of these groups can only be delivered
effectively with public assistance.
Although the need for dental public health
services is self-evident, there are still formidable
practical problems in making them available.
Public services in the United States, in contrast
to their counterparts in Canada and Europe, are
chronically underfunded. This is partly an off-
shoot of the individualist culture described ear-
lier, which leads to public services’ being held in
low esteem. The problem was exacerbated by
the severe cuts in public spending for social
services during the 1980s,13 cuts that have gone
even deeper since then and are causing new
lows in funding as states endure their financial
crises of the new century. Even when resources
are adequate, treatment for these special groups
is usually less efficient than it is for patients in
private practice. Oral health needs are often
greater, appointments can be missed if a patient
has a chance to earn some money instead of
going to the dentist, and the mentally or physi-
cally disabled just take more time to treat. Many
poor people change their place of residence fre-
quently in search of jobs, which makes continu-
ity of care impossible.
There is no simple answer to these problems,
though adequate funding of public health
departments would enable most of them to be
dealt with in time. Continuation of funding
would permit adequate staffing and equipment
levels, acceptable clinical facilities, special trans-
port where necessary, and community outreach
programs to educate the special groups on the
benefits of dental care. Adequate funding for
public services would assist more dentists and
hygienists to receive special training than is pos-
sible at present, so that in time the care received
by these diverse groups would approach that
received by mainstream America. Public treat-
ment programs do not present a threat to pri-
vate practice, for they aim to care for a different
patient.
REFERENCES
1. American Association of Public Health Dentistry. Code
of ethics and standards of professional conduct,
website: http://www.aaphd.org/prof/prac/law/code/
index.asp. Accessed October 10, 2003.
2. American Dental Association, Council on Bylaws and
Judicial Affairs. Principles of ethics and code of profes-
sional conduct. J Am Dent Assoc 1982;105:493-5.
3. American Dental Association, Council on Ethics,
Bylaws, and Judicial Affairs. Principles of ethics and
code of professional conduct. J Am Dent Assoc
1988;117:657-61.
4. American Dental Association, Council on Ethics,
Bylaws, and Judicial Affairs. ADA Principles of Ethics
and Code of Professional Conduct, website: http://
www.ada.org/prof/prac/law/code/index.asp. Accessed
September 26, 2003.
5. American Dental Hygienists’ Association. Code of
ethics for dental hygienists, website: http://www.
adha.org/aboutadha/codeofethics.htm. Accessed Sep-
tember 26, 2003.
6. American Public Health Association. Public health
code of ethics, website: http://www.apha.org/code-
ofethics/ethics.htm. Accessed October 10, 2003.
7. Banta D. What is health care? In: Jonas S, ed: Health
care delivery in the United States. 1st ed. New York:
Springer, 1977:12-39.
8. Beauchamp TL, Childress JF. Principles of biomedical
ethics. 5th ed. New York: OUP, 2001.
9. Billington RA. Frontiers. In: Woodward CV, ed: The
comparative approach to American history. New York:
Basic Books, 1968:75-90.
10. Camenisch PF. The moral foundations of scientific
ethics and responsibility. J Dent Res 1996;75:
825-31.
11. Cooke A. America. New York: Knopf, 1974.
12. Dentist must pay $100,000 to settle HIV case. ADA
News, 1994:Oct 3.
13. Evans CA. A national survey of public health dental
services in local health departments. J Public Health
Dent 1984;44:112-9.
14. Frankel MS. Developing ethical standards for responsi-
ble research. J Dent Res 1996;75:832-5.
15. Friedman JW, Atchison KA. The standard of care: an
ethical responsibility of public health dentistry. J Public
Health Dent 1993;53:165-9.
16. Fuchs V. Who shall live? Health, economics, and social
choice. New York: Basic Books, 1974.

17. Gaston MA, Brown DM, Waring MB. Survey of ethical
issues in dental hygiene. J Dent Hyg 1990;64:216-23.
18. Illich I. Medical nemesis: The expropriation of health.
New York: Bantam Books, 1976.
19. McCarthy CR. Legal and regulatory considerations con-
cerning research involving human subjects. J Dent Res
1980;59(Spec Issue C):1228-34.
20. Mitscherlich A, Mielke F. Doctors of infamy: The story
of the Nazi medical crimes. New York: Schuman, 1949.
21. Nash DA. A tension between two cultures. Dentistry as
a profession and dentistry as a proprietary. J Dent Educ
1994;58:301-6.
22. Ozar DT. A framework for studying professional ethics.
J Am Coll Dent 1991;58:4,6-9.
23. Proceedings of the IADR Council meeting. J Dent Res
1994;73:1289-94.
24. Shah RM. Introduction: Proceedings of a symposium,
Ethics in dental research. J Dent Res 1994;74:1757-8.
25. US Department of Health, Education, and Welfare,
National Commission for the Protection of Human
Subjects of Biomedical and Behavioral Research. The
3 Ethics and Responsibility in Dental Care 35
Belmont Report, April 18, 1979, website: http://www.
dhhs.gov/ohrp/humansubjects/guidance/belmont.
htm. Accessed February 15, 2004.
26. US Public Health Service, National Center for Health
Statistics. Population without health insurance,
1984–2001, website: http://www.cdc.gov/nchs/data/
hus/tables/2003/03hus129.pdf. Accessed October 10,
2003.
27. Weinstein BD. Ethics and its role in dentistry. Gen Dent
1992;40:414-7.
28. Woodward CV. The comparability of American history.
In: Woodward CV, ed: The comparative approach to
American history. New York: Basic Books, 1968:
3-17.
29. World Medical Association. Declaration of Geneva
(1948), website: http://www.cirp.org/library/ethics/
geneva/. Accessed September 26, 2003.
30. World Medical Association. Policy: World Medical
Association Declaration of Helsinki, 1964, with
amendments to 2002, website: http://www.wma.net/
e/policy/b3.htm. Accessed November 6, 2003.
 4 The Practice of Dental Public Health
WHAT IS PUBLIC HEALTH?
Identifying a Public Health Problem
DEVELOPMENT OF PUBLIC HEALTH IN THE
UNITED STATES
DENTAL PUBLIC HEALTH
Collection and Use of Data in Dental Public
Health
Public health is one of those aspects of life that
most people take for granted, or more likely
don’t think about at all. We take for granted that
we can drink a glass of water without thinking
about cholera, choose a restaurant without con-
cern about rats in the kitchen, and buy a can of
vegetables without worrying about botulism.
The source of the occasional outbreak of food
poisoning is rapidly identified by the authori-
ties, and thoughts of scarlet fever, typhoid, and
poliomyelitis simply never enter our heads. To
many of the younger generations, dental caries
is almost as distant as those infectious diseases
of the past. But this happy state of affairs has
not just happened; rather, it is the end point of
years of public health research and practice.
The low profile of public health has both
good and bad aspects. Although it is good that
mostly invisible basics like drains, sewage treat-
ment, fluoridated drinking water, and immu-
nizations against infectious diseases are part of
the accepted institutions of modern life, it is not
good that most people have so little grasp of
how public health functions. It is not good
because, without a constituency to press for it,
funding and legislation for public health can be
eroded, with subsequent threats to health and
the quality of life. By way of contrast, everyone
is acutely conscious of access, or lack of it, to
personal health services, and that subject is a
constant political issue. As is described later,
development of the public health infrastructure
36
Issues in Dental Public Health
DIFFERENCES BETWEEN PERSONAL AND
COMMUNITY HEALTH CARE
has taken a long time and has required some
painful lessons in lifting our quality of life to its
present level.
The purpose of this chapter is to examine the
structure and practice of dental public health in
the United States and to develop the theme that
dental public health and private dental practice
need to work together for the good of the com-
munity’s oral health.
WHAT IS PUBLIC HEALTH?
Health is an elusive concept to define. The World
Health Organization (WHO) definition64 is
often quoted. It states that “health comprises
complete physical, mental, and social well-being
and is not merely the absence of disease.” Noble
indeed, but too idealistic to be of much practical
value. A sociologist’s more pragmatic definition
is that health is “a state of optimum capacity for
the performance of valued tasks.”37 This is a
more useful definition in that it presents health
as a means to an end, that of maximizing the
quality of life, rather than as an end in itself.
Public health, too, does not lend itself to easy
definition. Among the many definitions that
have been formulated, Winslow’s is the
most widely accepted and quoted. Winslow
defined public health as “the science and art of
preventing disease, prolonging life, and pro-
moting physical health and efficiency through
organized community efforts.”63 The generality

of Winslow’s definition has much to do with its
widespread acceptance; however, it still pro-
vides little working knowledge of public health.
A more businesslike definition is “the organiza-
tion and application of public resources to pre-
vent dependency which would otherwise result
from disease or injury.”39 In this context,
dependency is defined as a condition in which
external resources, such as an attendant or med-
ication, are required for the individual to carry
out the routine activities of daily living. Just as
some definitions of public health can be vague
and idealistic, however, this one might go too
far in viewing dependency as the only outcome
to be avoided. Public health should deal with
quality-of-life conditions, rather than just those
that result in death or dependency, when it is
economically reasonable to do so.
A more useful definition of the public health
mission, one that accepts health as a means
rather than an end, is “fulfilling society’s inter-
est in assuring conditions in which people can
be healthy.”23 That seems to encompass every-
thing from maintaining the stratospheric ozone
layer to picking up the garbage to providing
recreational facilities, decent housing, or dental
care where needed. This definition might have
been ahead of its time in stressing the public
responsibility for a healthy physical and social
environment, while still leaving some room for
personal choices (“... in which people can be
healthy”).
The landmark 1988 report of the Institute of
Medicine (IOM), from which the last definition
came, went on to describe the functions of pub-
lic health agencies as the following:
●
Assessment. The regular collection and dis-
semination of data on health status, com-
munity health needs, and epidemiologic
issues.
●
Policy development. Promotion of the use of
the base of scientific knowledge in decision
making on policy matters affecting the
public’s health.
●
Assurance. The provision of services neces-
sary to achieve mutually agreed-upon
goals, either directly, by encouraging other
entities to supply them, or by regulation.23
These three domains have become the founda-
tion for evaluating many aspects of the public
health mission. The 1988 IOM report concen-
trated primarily on the role of governmental
4 The Practice of Dental Public Health 37
agencies in public health, and it came up with
the somber conclusion that the public health
system in the United States was “in disarray,”
deficient in many areas: availability of trained
personnel, communications, networking, and
of course funding. The IOM’s follow-up assess-
ment in 2002 found that too many of those
problems were still present.24
This 2002 IOM report incorporated the
broader, more inclusive view of public health
that emerged with the new century. This view
states that, although governmental agencies
remain the backbone of the public health sys-
tem, they cannot and should not do the job
alone.24 The IOM report goes beyond the tradi-
tional view of individual responsibility for
health and bases its recommendations on the
concept of population health, alluded to in the
1988 IOM definition but not clearly spelled
out. Population health is defined as “the health of
a population as measured by health status indi-
cators and as influenced by social, economic,
and physical environments, personal health
practices, individual capacity and coping skills,
human biology, early childhood development
and health services.”24
The essence of understanding population
health is grasping that people’s health is a func-
tion of more than just biology and other indi-
vidual clinical factors. People influence, and are
influenced by, the values and beliefs of the
broader community in which they live and
work. To illustrate, exhorting a person to stop
smoking is likely to be fruitless if everyone in
that individual’s world smokes and smoking is
an important part of the person’s social interac-
tions. Attempts to persuade a person to eat
more vegetables will fail when the social envi-
ronment calls for a diet of deep-fried foods or
when local food stores do not stock the needed
items. All of this means that, in the promotion
of public health, the governmental public
health agencies need to coordinate with com-
munity-based organizations, the health care
delivery system, academia, business, and the
media if good population health is to be
achieved. A shift of the mindset more toward
population health and away from purely indi-
vidual health could help the United States
reduce anomalies such as expenditure of 95%
of health care dollars on medical care and bio-
medical research when there is evidence that
38 Dentistry and the Community
behavior and environment are responsible for
70% or more of avoidable mortality.24 The
United States is easily the world leader in health
care expenditures, but its scores on health status
measures are well down in the list. A shift in
where we invest our health care resources would
help redress that imbalance, though this is not
easy in a society in which individualism is dom-
inant (see Chapter 3).
The core of public health practice is shown in
Box 4-1, which presents a succinct definition of
the mission and essential services that only
public health can provide. This statement,
developed by the American Public Health
Association in 1994, has since received virtually
universal acceptance.
Identifying a Public Health Problem
Ask people in the street whether they consider
human immunodeficiency virus (HIV) or West
Nile virus a public health problem, and most
will give a resoundingly affirmative reply. What
about deaths from traffic accidents? There will
be more equivocation, even though the number
of deaths from road accidents in 2000 was three
times higher than that from HIV-related dis-
ease.58 Substance abuse similarly is seen by
BOX 4-1 Essential Public Health Services in the United States3
Vision: Healthy people in healthy communities.
Mission: Promote physical and mental health and
prevent disease, injury, and disability.
What Public Health Does: The Purpose of Public
Health
●
Prevents epidemics and the spread of disease.
●
Protects against environmental hazards.
●
Prevents injuries.
●
Promotes and encourages healthy behaviors and
mental health.
●
Responds to disasters and assists communities in
recovery.
●
Assures the quality and accessibility of health
services.
How Public Health Serves: The Practice of Public
Health
●
Monitors health status to identify and solve
community problems.
most as a major social and public health prob-
lem, but fewer would view infant mortality as
such a problem, even though the United States
had only the twenty-eighth lowest infant mor-
tality rate globally in 1999.59 So, given that
handling a public health problem demands
some allocation of resources and some oppor-
tunity costs, how is a public health problem
determined?
Over the years some criteria have emerged
for its definition. Blackerby, for example,
listed them as the following: (1) a condition
or situation that is a widespread cause of mor-
bidity or mortality, (2) there is a body of
knowledge that could be applied to relieve the
situation, and (3) this body of knowledge is
not being applied. 10 However, these criteria
seem unduly restrictive. For example, the
Black Death in the fourteenth century killed
off one third of the population of Europe in 3
years. There is no question that it was a public
health problem, even though there was no
body of knowledge on how to deal with it.
Subsequent epidemics of typhoid, cholera, yel-
low fever, and other infectious diseases were
also public health problems before there were
effective means to deal with them, and the same
●
Diagnoses and investigates health problems and
health hazards in the community.
●
Informs, educates, and empowers people about health
issues.
●
Mobilizes community partnerships and action to
identify and solve health problems.
●
Develops policies and plans that support individual
and community health efforts.
●
Enforces laws and regulations that protect health and
ensure safety.
●
Links people to needed personal health services and
assures the provision of health care when otherwise
unavailable.
●
Assures a competent public and personal health care
workforce.
●
Evaluates effectiveness, accessibility, and quality of
personal and population-based health services.
●
Researches for new insights and innovative solutions
to health problems.

can be said for some viral infections today. The
nonapplication of effective treatment for a
problem, as suggested by Blackerby,10 is more a
breakdown in public organization, funding and
personnel resources, or political will.
Additional criteria can broaden the scope of
what constitutes a public health problem.
Public perception is one, as in the earlier exam-
ple of the HIV epidemic. If enough of the public
perceive a public health problem, then the
mandate exists to allocate resources to deal with
it. HIV is in that category (even though the only
means to prevent its spread, apart from the bar-
rier precautions in medical and dental practice,
are behavioral modifications). Not only public
perception, but governmental perception, goes
far toward defining a public health problem.
When a government assigns a problem to its
public health agency for attention, virtually by
definition it is a public health problem. If a
president, governor, or mayor defines a public
health problem by decree, then a public health
problem it is, whether or not public health pro-
fessionals agree. These latter two types of deci-
sion, legislative mandate and executive order,
can have the advantage of ensuring immediate
action as well as the potential disadvantage of
disturbing the orderly process of program plan-
ning and operation.
Today, we can define a public health problem
as an issue that meets the following criteria:
●
A condition or situation is a widespread
actual or potential cause of morbidity or
mortality.
●
There is a perception on the part of the
public, government, or public health
authorities that the condition is a public
health problem.
To use cigarette smoking as an illustration, the
first condition has been satisfied based on the
first report of the Surgeon General of the United
States in 1964,53 and there is no question that
the second condition has also been met. These
criteria have also been met for the HIV epi-
demic. Allocation of public resources to deal
with a recognized problem is a logical conse-
quence, although not a criterion for problem
recognition. In the case of cigarette smoking,
there has been considerable action through
widespread public education campaigns, adver-
tising bans, and efforts to block the sale of ciga-
rettes to minors. On the other hand, the public
4 The Practice of Dental Public Health 39
is divided about condom distribution and
needle-exchange programs intended to inhibit
the spread of HIV infection.36
DEVELOPMENT OF PUBLIC HEALTH
IN THE UNITED STATES
Early public health practice in the colonies on
the eastern seaboard naturally reflected the
English experience. The first English Poor Laws,
dating from the seventeenth century, put the
burden of caring for the disadvantaged on the
local community. This was rational enough
in an agrarian society when people didn’t
move around. However, when the Industrial
Revolution took hold in Britain during the late
eighteenth century the Poor Laws broke down,
for industrialization was really a massive social
revolution.51 Mass migration to the cities cre-
ated overcrowding, disease, and epidemics,
while the laissez-faire economic attitudes of the
time led to great wealth for some, the emer-
gence of a middle class, and appalling squalor
for many. The Poor Laws, which dealt only with
the relief of destitution, were not designed for
these completely new kinds of social and health
problems.
The ideology of laissez-faire economics in
Victorian Britain, combined with an acceptance
of Malthusian theories of population growth,
led to only grudging action to improve the lot of
the destitute. Malthus, a nineteenth-century
English country clergyman, wrote that unre-
stricted growth of population would eventually
exceed the expansion of the food supply.32 The
growth of population therefore needed to be
checked, either by “moral restraint” or by the
inroads of starvation, disease, or other disasters,
which Malthus grouped under the cheerful
heading of “misery and vice.” Public attitudes at
the time were such that Malthus struck a sympa-
thetic chord with his views that terrible living
conditions were not the result of uneven socioe-
conomic development but rather the conse-
quence of necessary natural laws. Given these
views, new public welfare programs that were
degrading to their recipients were perceived as
being in the public interest as well as morally
justified.
Although British provision of health services
subsequently turned full circle to the establish-
ment of a National Health Service in 1948,
40 Dentistry and the Community
these condescending views on public health
and welfare were the norm when organized
public health development began in the United
States during the nineteenth century. It was an
environment in which public health could not
grow much beyond attempts to limit the spread
of epidemics. Not surprisingly, nineteenth-
century industrialization produced the same
pattern of social turbulence in the United States
that had occurred earlier in England.13 At a local
level, similar upheavals are seen today, when
the abrupt closure of an industry can blight the
vacated community. These disruptions take
place now in a highly mobile society, in which
the old Poor Law approach that local communi-
ties should be fully responsible for public
assistance is clearly obsolete. In modern-day
industrial and postindustrial society such prob-
lems are national in scope and should be
treated that way.
One reason why the modern American
approach to public health and welfare differs
from the current British model is that the stern
puritan views of the early European settlers have
had a more sustained influence on public pol-
icy in the United States than they did in Britain
and Europe. One expression of the puritan ethic
in the United States was that general welfare
relief and payment for health care services for
the indigent remained linked together longer
than they did in European countries, which
compounded rather than disentangled the prob-
lems.49 When this is added to the American cul-
ture of individualism and the relative freedom
from the wartime cycle of social disruption and
reform, we can see why communal attitudes
toward health and environment have never
really flourished in the United States (see
Chapter 3).
Dentistry did not play a significant part in
the early development of public health in the
United States. Oral health was of little concern
at a time when the population was decimated
periodically by typhoid, diphtheria, cholera,
smallpox, and gastroenteric diseases. Although
a few public clinics were established on a volun-
tary basis by dentists as early as the mid-
nineteenth century, public dental care facilities
remained almost nonexistent for many years.42
The U.S. Public Health Service, for example, did
not employ dentists on a regular basis until
1919,43 and philanthropic dental clinics such as
Eastman, Forsyth, Guggenheim, Mott, and
Strong-Carter all opened between 1910 and
1930.
DENTAL PUBLIC HEALTH
Dental public health is one of the nine board-
certified specialties of dentistry in the United
States and was certified in 1950. The American
Board of Dental Public Health adapted
Winslow’s definition to develop one subse-
quently approved by the American Association
of Public Health Dentistry, the Oral Health sec-
tion of the American Public Health Association,
and the American Dental Association (ADA).
That definition is as follows:
Dental public health is the science and art of pre-
venting and controlling dental diseases and promot-
ing dental health through organized community
efforts. It is that form of dental practice which serves
the community as a patient rather than the individ-
ual. It is concerned with the dental education of the
public, with applied dental research, and with the
administration of group dental care programs as well
as the prevention and control of dental diseases on a
community basis.2
Implicit in this definition is the requirement
that the specialist have broad knowledge and
skills in program administration, research
methods, the prevention and control of oral dis-
eases, and the methods of financing and provid-
ing dental care services. Box 4-2 is the dental
corollary of the essential public health func-
tions summarized in Box 4-1, a concise listing
of the essential functions of dental public
health (sometimes referred to as core functions)
as adopted by the Association of State and
Territorial Dental Directors (ASTDD).
Dentists and dental hygienists have entered
the dental public health field when they are
employed in the administration of public
health programs (which can include health pro-
motion, community prevention, and provision
of dental care to specified groups); become fac-
ulty members in departments dealing with
community-oriented dental practice; or become
researchers in epidemiology, prevention, or
provision of health services. Some researchers
in the behavioral sciences related to dental
health can also be considered public health per-
sonnel. Dentists become recognized specialists
when, in addition to being employed full time

BOX 4-2 Essential Public Health Services to Promote Oral Health in the United States4
I. Assessment
A. Assess oral health status and needs so that
problems can be identified and addressed.
B. Analyze determinants of identified oral health
needs, including resources.
C. Assess the fluoridation status of water systems
and other sources of fluoride.
D. Implement an oral health surveillance system to
identify, investigate, and monitor oral health
problems and health hazards.
II. Policy Development
A. Develop plans and policies through a
collaborative process that support individual and
community oral health efforts to address oral
health needs.
B. Provide leadership to address oral health
problems by maintaining a strong oral health unit
within the health agency.
C. Mobilize community partnerships between and
among policy makers, professionals, organizations,
groups, the public, and others to identify and
implement solutions to oral health problems.
in the fields mentioned, they achieve diplomate
status with the American Board of Dental Public
Health. Specialty certification first requires sat-
isfaction of the educational requirements of the
Council on Dental Education of the ADA (i.e.,
2 years of accredited advanced graduate educa-
tion in the specialty, plus fulfillment of a work
experience requirement, and then completion
of the specialty board examinations).
Although there are fewer than 200 board-cer-
tified specialists in dental public health, the spe-
cialty’s influence on the oral health of the
public is greater than those numbers would sug-
gest.1 Dental public health professionals are
employed by federal, state, and local health
departments, conduct research in universities
and government agencies, and are administra-
tors in professional organizations and various
foundations. Dental public health practice gets
away from the relative isolation of the dental
office, for its programs require cooperative
effort with other professionals such as physi-
cians, nurses, engineers, social workers, and
nutritionists. Among the rewards is the ability
to bring about improvement of the oral health
4 The Practice of Dental Public Health 41
III. Assurance
A. Inform, educate, and empower the public
regarding oral health problems and solutions.
B. Promote and enforce laws and regulations that
protect and improve oral health, ensure safety, and
ensure accountability for the public’s well-being.
C. Link people to needed population-based oral
health services, personal oral health services, and
support services, and ensure the availability,
access, and acceptability of these services by
enhancing system capacity, including directly
supporting or providing services when necessary.
D. Support services and implementation of programs
that focus on primary and secondary prevention.
E. Ensure that the public health and personal health
workforce has the capacity and expertise to
address oral health needs effectively.
F. Evaluate effectiveness, accessibility, and quality of
population-based and personal oral health services.
G. Conduct research and support demonstration
projects to gain new insights and applications of
innovative solutions to oral health problems.
status of whole populations rather than of sin-
gle patients. Public health dentists serving in the
Indian Health Service of the U.S. Public Health
Service, for example, have demonstrated over
the last generation their ability to upgrade den-
tal care for several million Native Americans
from a bare emergency service to comprehen-
sive care for many, carried out in excellent clini-
cal facilities. Similarly, a dental public health
professional who institutes water fluoridation
in a community has done more for its oral
health than could be achieved in a lifetime of
private dental practice.
Achievements of dental public health profes-
sionals include conducting the epidemiologic
studies that established the basis for commu-
nity water fluoridation, carrying out clinical tri-
als to demonstrate the effectiveness of fluoride
toothpastes and other products, and imple-
menting the associated caries-control programs,
which have been fundamental to the decline in
caries among children.1 Oral epidemiologists
have also charted the natural progression of
periodontal diseases7 and are beginning to
assess other oral conditions about which little is
42 Dentistry and the Community
known. Administrators in dental public health
pioneered the concept of providing regular den-
tal care in a logical, sequential way for large
population groups,16,17,62 and they demon-
strated the increased productivity that efficient
use of dental auxiliaries brings to patient
care.31,38 Dental hygienists have proved their
value in dental public health well beyond their
traditional role as educators. Hygienists act as
directors of sealant teams and members of epi-
demiologic survey teams, and serve in several
capacities in the growing field of special pro-
grams for the elderly.
To round out this discussion of what dental
public health is, it might be useful to state what
it is not. It is not just “dentistry for the poor,”
although provision of care to persons who do
not fit the private practice mode is part of it. It is
not just “Medicaid dentistry,” although improv-
ing that creaky and inefficient program is of
concern to all health professionals. It is not just
conducting surveys of oral health, although
monitoring disease trends and collecting data
for program planning and evaluation is an inte-
gral part of public health practice. It is not just
fluoridation, though dental public health has
always been in the front line with regard to that
public health measure. Similarly, dental public
health is not “socialized dentistry,” health
maintenance organizations, preferred provider
organizations, Occupational Safety and Health
Administration regulations, infection control,
quality assurance, financial support (or lack of
it) for dental education, or expansion of func-
tions for dental auxiliaries. And public health is
not just the provider of last resort. Its function
goes well beyond filling the health care gaps for
those whom the private sector cannot or will
not treat.
Simply put, dental public health is concern
for, and activity directed toward, the improve-
ment and protection of the oral health of the
whole population. Narrowing the role of dental
public health only to groups defined as high
risk or underserved would exclude such basic
activities as the efforts to control tobacco expo-
sure, infection control in dental practice, and
water fluoridation.14 Because organized den-
tistry also espouses the goal of optimum oral
health for all, public and private sectors need to
understand each other and work cooperatively
if this worthy goal is to be achieved.
Collection and Use of Data in Dental
Public Health
Information on health conditions is fundamen-
tal to public health practice, and the necessary
data can be collected in different ways. Data on
vital statistics, plus information on certain infec-
tions that could become epidemics, are gathered
by a process known as surveillance. Surveillance
in public health is the ongoing systematic collec-
tion, analysis, and interpretation of outcome-
specific data for planning, implementation, and
evaluation of public health practice.50 It is an
ongoing data collection system which uses
methods that are quick, simple, and practical
and are designed to put as little burden as possi-
ble on the busy health professionals who do the
reporting. As a result, the data are usually not as
accurate as those collected under a strict proto-
col in research projects, but they are seen as
accurate enough for disease monitoring. This is
a key concept in public health: data for planning
and evaluation, although they must be valid, do
not need to be as precise as data in clinical trials.
Some data are always better than no data, and
the collection of data for public health purposes
needs a collection protocol that emphasizes
practicality and reliability rather than total preci-
sion. One must remember that the main pur-
pose of surveillance is to detect changes in
trends or distribution of disease so that inves-
tigative or control measures can be initiated if
needed. Surveillance is a finger on the pulse of
the public’s health.
In the United States, surveillance activities at
the state and local level are coordinated by the
Epidemiology Program Office at the Centers for
Disease Control and Prevention (CDC) in
Atlanta. Guidelines are available for evaluating
surveillance systems.57 Perhaps the best known
of these surveillance systems is the Surveillance,
Epidemiology, and End Results (SEER) program
for cancer reporting. SEER is the source of virtu-
ally all cancer data in the United States (see
Chapters 18 and 23), including oral cancer.
Data sources for surveillance activities
include the following:
●
Vital statistics (e.g., births, deaths)
●
Information on reportable diseases (e.g.,
plague, cholera, yellow fever, and others
designated by states)
●
Registries (e.g., congential defects, cancer)

●
Administrative data collection systems
(e.g., hospital discharge data)
Information is mostly collected by passive
surveillance, which means that, although
physicians and hospitals are required to notify
appropriate authorities whenever reportable
conditions are encountered, the authorities
themselves do not actively solicit such data.
Some errors of omission undoubtedly occur as
a result. On some occasions, health department
staff go into the field to collect data, often on a
specific disease, for a limited time. The staff peo-
ple call physicians and hospitals, by arrange-
ment, to obtain data on new cases and to get
demographic and other relevant data. This
process is known as active surveillance and is
similar to investigating an outbreak of an infec-
tious disease.
Until recently, the absence of a surveillance
system for oral conditions (other than oral can-
cer, which is included in cancer registries, and
cleft lip and palate, for which some states have
registries) hampered the development of tar-
geted approaches to improve oral health.
Surveillance in dental public health had been
largely restricted to surveys, in which samples of
a defined population are examined clinically or
assessed by questionnaire. Surveys, which have a
lot in common with active surveillance, range in
scope from large national surveys conducted by
federal agencies (see Chapters 19–22), to
statewide surveys,41 to local community surveys
conducted by a state or local public health
agency.46 Important though they are, surveys
involving clinical examinations can be too
expensive and logistically demanding for most
state or local agencies. National surveys, con-
ducted by the National Center for Health
Statistics and in the past by the National
Institute of Dental (and Craniofacial) Research,
provide excellent clinical data for the whole
nation, but state-level data cannot be pulled out
because the sampling system is not so designed.
A sampling system that permits extraction of
state-level data is possible but would be too
expensive for the budget of the National Center
for Health Statistics. National data do not work
well as a basis for local planning for the reasons
given in Box 4-3, and the future of extensive
clinical examinations in national surveys
is uncertain because of time and cost. More
reliance on true surveillance systems, in which
4 The Practice of Dental Public Health 43
useful data can be collected fairly inexpensively,
is needed.
A new approach came with the establishment
in the mid-1990s of the National Oral Health
Surveillance System, a joint venture of the CDC
and ASTDD.55 Although its full development
will take time, this is a historic enterprise in
that the traditional suspicion between the fed-
eral government and the states has now been
replaced by a cooperative federal-state arrange-
ment. States wanting to collect their own survey
data can now turn to the CDC for help with
financing and expertise, and quite a number
have done so. The result is that, within a fairly
short period, a number of states have collected
valuable data for planning and evaluation that
they otherwise would not have obtained.
The main focus of the National Oral Health
Surveillance System is on data for a set of eight
oral health indicators: dental visits, teeth clean-
ing (professional), complete tooth loss, fluori-
dation status, caries experience, untreated caries,
sealants, and oral cancer. The data themselves
are mostly state specific and mostly come from
several state-based surveys, of which the most
used are the Behavioral Risk Factor Surveillance
System (BRFSS)56 and its companion Youth
Risk Behavior Surveillance System (YRBSS). In
these telephone surveys, the core questionnaire
developed by the CDC can be adapted by a state
health agency for its local needs. Use of chewing
tobacco is one example of a topic about which
some states want information when the habit is
known to be a problem, whereas other states do
not. The BRFSS telephone surveys began in the
early 1980s, and by 1994 all states and territo-
ries were participating. These two surveys are the
basis for current data on four of the oral health
indicators: dental visits, teeth cleaning, com-
plete tooth loss, and fluoridation status.55
Some state dental directors have already con-
ducted statewide oral health surveys with CDC
assistance; others are planning to do so. Having
both statewide clinical data and BRFSS data
gives a state an excellent view of conditions
when preparing an oral health plan.
National surveys that include a clinical den-
tal examination of the participants usually
involve performance of a lengthy and detailed
clinical examination, a type of examination
that states could not handle because of the
cost—time is money in dental public health as
44 Dentistry and the Community
BOX 4-3 Problems Related to the Use of National Surveys As a Type of Surveillance9
National surveys that include clinical dental
examinations, such as those conducted by the National
Center for Health Statistics, provide a superb data set
on oral conditions. The data are collected by trained
examiners, and the representative sampling ensures
that the data are generalizable to the national
population. National surveys are not true surveillance,
however, and reliance on them as a type of surveillance
brings its problems. These can be listed as follows:
●
Reliance on primary data collection comes from
the underlying view that only trained dental
professionals can record oral disease. Experience
with the use of death certificates, which are
completed by all sorts of untrained persons
following standard protocols, is just one example
which implies that the traditional attitude has
become a dinosaur.
●
The protocol for national surveys was developed
primarily to record dental caries. However, caries
continues to decline, and other conditions are
becoming of more concern. In addition, the
recording of past disease (restorations and
extracted teeth), rather than just present disease,
does not fit the philosophy of surveillance and may
even be invalid.
it is anywhere else. Hence, this increased activity
in collecting state-level oral health data has
been stimulated by the development of quick
and simple data collection protocols—again we
see the underlying principle of making surveil-
lance as practical as possible, even at the
expense of precision.
The first major step toward practical oral
health surveillance came in the mid-1990s, when
the ASTDD developed a seven-step model for
state and local agencies for collecting dental
data by choosing from a variety of approaches
to best suit local needs.45 This model includes
the planning process, identification of partner
organizations, determination of whether new
data collection (clinical examinations, tele-
phone surveys, questionnaires) is needed or
whether existing data will do, and prioritization
of the issues that arise from the collected infor-
mation. For new data collection (step 4 in the
seven-step program), a basic screening survey,
plus a training program to use it effectively, has
been developed by the ASTDD.5 Again, the prin-
●
Examination protocols record data at the surface
level (caries) and at up to six sites per tooth
(periodontitis). However, oral health objectives are
stated with the individual person as the unit of
measurement, so all that time and effort is
probably not well spent.
●
There is no good surveillance tool to measure
periodontal diseases. Despite all the detailed
indexes of periodontal diseases (see Chapter 16),
we cannot yet identify a person with active
progressing disease.
●
Visual-tactile clinical examinations in national surveys
consume a lot of resources—they are expensive.
●
Public participation in surveys of representative
samples of population is diminishing. This
problem is severe enough in some instances to
introduce response bias—the people who do
participate are different in some way from those
who do not. This weakens the generalizability of
the results, one of the chief reasons for conducting
such surveys.
●
The sheer logistics of national surveys means that
data are nearly always reported late, sometimes
years late. More timely data are needed for public
health authorities to plan and evaluate programs.
ciple behind the basic screening survey is to per-
mit limited but valid clinical data to be collected
as efficiently and unobtrusively as possible.
WHO has developed and systematized basic
methods of data collection for surveillance of
oral conditions in all parts of the world into an
approach known as Pathfinder.66 Although not
all details of these methods have received uni-
versal acceptance (see Chapter 16), WHO has
succeeded very well in promoting the collection
and use of data in parts of the world where pre-
viously there was no information at all on oral
conditions. The simplicity of the protocol for
sampling and data collection permits it to be
used by dental personnel with no previous
training in survey methods. The country-
specific data collected by Pathfinder and other
survey methods are maintained in WHO’s
Global Oral Data Bank.65
By whatever method they are collected, den-
tal data are used to identify needs and to plan
programs to meet those needs. Functioning pro-
grams then need to be evaluated. The results of

Collection of information
Evaluation Establishment of
long-term goals
Implementation of Specific objectives
programs
Strategic planning:
selection of programs
Fig. 4-1 The planning cycle.
evaluation can lead to plan modifications, and
so the cycle continues. This ongoing process is
known as the planning cycle and is illustrated in
simplified form in Fig. 4-1.
Data from surveys or surveillance are part of
the foundation on which public policy at fed-
eral, state, and local levels is built. Some federal
funding programs for dental public health, such
as the Maternal and Child Health block grants,
require that needs assessment and planning
data be submitted each year with a state’s appli-
cation for funds. Agencies and foundations that
fund research use oral survey data to help estab-
lish their research priorities; dental schools use
them when establishing curricula; state agencies
can use them in regulating the activities of den-
tists and hygienists; and dental insurance com-
panies consult them when establishing benefit
packages.
We now look at two issues that are major
concerns for all of dentistry in the early twenty-
first century but that are of particular concern to
public health dentistry.
Issues in Dental Public Health
Access to Care
The highest public health post in the country is
that of Surgeon General of the United States.
In 2000, the Surgeon General at the time,
Dr. David Satcher, published a landmark report
on oral health in America.52 Although there had
4 The Practice of Dental Public Health 45
been many previous Surgeon Generals’ reports
on various aspects of public health in the past,
this was the first report devoted to oral health.
This comprehensive and detailed review of all
aspects of oral health hammered two principal
themes throughout:
1. There are substantial disparities in oral
health status between upper and lower
socioeconomic groups; between the white
mainstream and racial-ethnic minorities;
between the insured and uninsured; and
between suburban areas and inner city
and rural areas.
2. Poor access to care is a major barrier in
eliminating these disparities.
Access to care refers to whether or not a person
can obtain needed care. In dental care, it
involves the following:
●
Is there a dental office physically available
within a reasonable distance and open at
reasonable times?
●
Is there transportation to this dental office?
●
Does the person have the financial resources,
either on his own or through insurance, to
pay for dental treatment?
●
Can the person take the time to go to the
dentist without jeopardizing his job?
If the answer to these four questions is not
“yes,” then the person has access to dental care
that is restricted, at least to some degree.
Dentists in general, and public health den-
tists in particular, have been aware of the access
problem for years. The federal government has
also been involved in the issue for years, though
not always with great success. Federal programs
for Medicaid and designation of dental health
professional shortage areas are discussed more
fully in Chapters 7 and 8.
Health centers are an approach to improving
dental care access for all people that is having
some success. Some health centers have been
around since the enabling legislation in 1965,
and now federal funding assistance is available
for community health centers, migrant health
centers, programs providing health care for the
homeless, and public housing primary care pro-
grams that meet federal requirements for their
administration. Those that meet the require-
ments are known as federally qualified health
centers (FQHCs). There are some 670 such cen-
ters in the United States that are supported by
the Bureau of Primary Health Care in the federal
46 Dentistry and the Community
Health Resources and Services Administration.54
These centers, often referred to as “safety-net”
facilities, provide comprehensive care for some
11 million Americans. Care is not totally free,
and the centers have some local funding sources
and have community-based boards of directors.
Nearly 1000 dentists are employed in FQHCs.54
Dentists in public health are highly support-
ive of FQHCs, for they go a long way to reducing
access barriers for low-income people. Continu-
ing support of FQHCs will reduce the access
problem even further.
Should Preventive Strategies Be Targeted
or Population Based?
The idea of predictively identifying caries-suscep-
tible individuals was given renewed emphasis
with the decline in caries experience that became
evident during the 1980s (see Chapter 20). Most
caries and severe periodontitis is now found to be
concentrated in relatively small groups; that is, in
statistical terms these problems have a skewed dis-
tribution, which logically leads to the concept of
targeting these susceptible individuals in preven-
tive programs. Simply put, targeting means that it
is deemed more efficient for both practitioners
and public health administrators to focus preven-
tion efforts on the susceptible minority rather
than apply them across the board, including to
people who would not necessarily benefit (water
fluoridation is an important exception to this
philosophy). Targeted prevention is often
assumed to be more cost effective than a whole-
population strategy, although it has not yet been
demonstrated to be so. When administrative
costs and the costs of the predictive tests them-
selves are added, targeting may not always be the
most efficient approach. The issue is still the
subject of a spirited debate in dentistry, with argu-
ments for40 and against.6,22 An interactive com-
puterized approach (the “cariogram”) to assess
caries risk and demonstrate it graphically has
been evaluated for children21 and for an elderly
group,20 though how best to apply the cariogram
remains uncertain.
Most research into caries prediction has
been in microbiology, with tests based on the
assumption that high counts of Streptococcus
mutans and lactobacilli indicate high risk of sub-
sequent caries.28,44,48 Although the causative role
of these bacteria in caries is unquestioned,30
a direct association between bacterial counts and
caries incidence is found only within groups,
rather than for any one individual.25 Bacterio-
logic tests, in general, are highly specific,60 which
means that a low S. mutans count accurately pre-
dicts low caries experience; however, they have
less positive predictive value, that is, a lot of per-
sons who test positive with high S. mutans counts
will not develop caries (see Chapter 13).
Efforts have also been made to predict caries
susceptibility in the permanent dentition from
caries experience in the primary dentition.
Although some researchers have found correla-
tions, others have not, so this approach cannot
be recommended.61 The reason for the variable
correlations is probably that the caries-causing
factors during young childhood differ from
those in later years.
As caries incidence continues to decline in
the economically developed world, it becomes
more difficult to predict the susceptible minor-
ity in a population.26 It is also likely that the
cost effectiveness of public health efforts to
identify susceptible individuals will diminish as
the proportion of such individuals decreases.27
A combination of tests is more effective than
any single test,8 but the more tests used, the
higher the cost. One rationale for identifying
the highly susceptible individual is to improve
cost effectiveness by focusing preventive pro-
grams; thus, if it becomes too expensive to iden-
tify susceptible persons, that rationale collapses.
This is a vexing dilemma, and it inhibits target-
ing based on individual susceptibility. The
philosophical basis for research that equates
high disease status with high risk can also be
debated, for outcome cannot be used to deter-
mine risk34 and deterministic models do not
allow for random effects.33
So what should be done about targeting,
given that individual targeting is not efficient?
There is always the social dimension, which has
gained more attention in recent years. Caries is a
social disease, given that it has been related to
neighborhood characteristics such as the per-
centage who live in public rather than private
housing, rates of poliomyelitis vaccination,
car ownership rates, and degree of financial
problems.19 Evidence has long suggested that
socioeconomic status is as good a predictor of
group susceptibility to caries as any12,15,18,35 for
public health programs. This introduces the
idea of geographic targeting.11 In virtually any

jurisdiction there is always some area with poor
social conditions that can be selected for special
attention. States that conduct sealant programs,
for example, do not have the resources to go to
all schools in a state, so they choose target areas
based on the proportion of children eligible for
free or subsidized lunch. In Ohio, one such
state, the program does not attempt to select
out individual “high-risk” children from these
schools; all children in selected schools are eli-
gible for treatment where indicated. This is an
example of true geographic targeting—the
whole population is eligible within specific geo-
graphic boundaries. And it works—evaluation
results show that such programs have substan-
tially reduced the disparity in sealant placement
between children from low-income families
and those from higher-income families.47
New York also selects geographic areas for
its sealant program. The choice is based on
socioeconomic status, demonstrated need,
community interest, operational feasibility,
and ability to comply with the health depart-
ment’s rules and regulations.29 Evaluation
showed that the criteria for selection of indi-
vidual children and teeth were not well fol-
lowed by the sealant teams. This finding did
not mean that the sealant teams showed a cav-
alier disregard for the carefully designed crite-
ria; rather, their behavior was a necessary
response to pressures from parents and school
personnel that the sealant teams found diffi-
cult to resist. It indicates yet again that target-
ing of individuals is just difficult to do in
real-life situations.
DIFFERENCES BETWEEN PERSONAL
AND COMMUNITY HEALTH CARE
In addition to the similarities between private
and public health practice, there also are some
notable differences. It is fair to say that most
practitioners do not understand the goals of
public health. That is unfortunate, because both
privately and publicly employed dental profes-
sionals are working toward the same end: the
oral health of the public. At the philosophic
level, one major difference between personal
care and public health is that the goals of public
health are socially determined, whereas the pri-
orities of private care are only coincidentally
related to social goals. Another way of looking
4 The Practice of Dental Public Health 47
at this distinction is to say that private care seeks
to maximize the chance that the best outcome
will occur, often unlimited by resource restraints.
Public health, on the other hand, seeks to mini-
mize the chance that the worst outcome will
occur.39
The private practitioner works more or less
alone. Decisions the dentist makes are in the
context of his training, the legal framework
for dental practice, and the dentist-patient rela-
tionship. Despite insurance carriers, quality
assurance programs, and governmental require-
ments, the private practitioner is still a relatively
independent health care provider. By contrast,
the public health professional is a salaried
employee who is accountable to both an imme-
diate supervisor and to the taxpayers, repre-
sented in such forms as a board of health,
a community advisory board, and a governing
body. Rarely is a major decision in public health
made on one’s own.
The public health professional often works
in communities with special characteristics of
culture, language, socioeconomic status, and
values. Public health workers often must care
for those outside the mainstream, where
those characteristics just mentioned make
some groups of people more difficult and often
more expensive to reach. The challenge in den-
tal public health practice is that patients in these
groups often do not share middle-class values
with regard to brushing their teeth, keeping
appointments, or making regular dental visits,
but they still need care if the professional trust
of working for the oral health of the public is to
be preserved.
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18. Gillcrist JA, Brumley DE, Blackford JU. Community
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25. Kingman A, Little W, Gomez I, et al. Salivary levels
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28. Krasse B. Biological factors as indicators of future caries.
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29. Kumar JV, Wadhawan S. Targeting dental sealants in
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4 The Practice of Dental Public Health 49
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 5 Oral Health Promotion
WHAT IS HEALTH PROMOTION?
COMMUNITY-BASED HEALTH PROMOTION
PROMOTION OF ORAL HEALTH
GOALS FOR ORAL HEALTH
Is any individual’s health status solely her own
responsibility, or does society have some part to
play in it? We discussed this issue when defining
health in Chapter 4 and concluded that both
were involved. Put concisely, the individual is
responsible for the conduct of her life, but soci-
ety is largely responsible for the conditions of her
life.5 The achievement of health requires a set of
social conditions within which the individual
can then take actions that enhance health.85
This chapter discusses the promotion of oral
health in the community and among individual
patients. Issues of public policy that permit peo-
ple to maximize their oral health are considered
and some examples of major community-based
health promotional interventions are assessed.
Because cultural values strongly influence
health promotion, public and professional atti-
tudes and beliefs are also examined. As an
example of how health promotional principles
might be applied at the community level, the
role of health professionals in promoting water
fluoridation is assessed. We do not go into
details of educational theory in this chapter;
a number of excellent texts provide such
details.39–41,83
WHAT IS HEALTH PROMOTION?
Community health promotion is defined as any
combination of educational, social, and envi-
ronmental actions conducive to the health of a
population of a geographically defined area.39
Another definition is that health promotion is a
50
KNOWLEDGE AND ATTITUDES ABOUT ORAL
HEALTH
DENTAL HEALTH EDUCATION
PROMOTION OF WATER FLUORIDATION
set of processes that can be employed to change
the conditions that affect health, so that targets
are not always the people whose health is in
question.83 Yet another simply states that
health promotion is the process of enabling
people to increase control over, and to improve,
their health.101 These definitions all envision
roles for the health professional, political lead-
ers, society as a whole, and the individual in
maximizing health status. Health education is
an important part of health promotion, though
it is just one part of the larger entity. Health
education is defined as any combination of
learning opportunities designed to facilitate
voluntary adaptations of behavior that are con-
ducive to health.38 Health education and health
promotion have been described as the mecha-
nisms that connect prevention activities, policy
development, and program implementation,
maintenance, and evaluation.31
Although health is an elusive entity to define,
we stated in Chapter 4 that it is more than
the mere absence of disease and less than
the idealistic definition of the World Health
Organization (WHO). Greenberg refers to
health as a quality of life with social, mental,
emotional, spiritual, and physical functions,41
and he points out that too much emphasis is
usually given to the physical function at the
expense of the others. In effect, Greenberg
is arguing for a “holistic” view of health. He
defines wellness as a positive state, the degree
to which a person has reached her potential
regarding each of the components of health.

Because it is the integration of social, mental,
emotional, spiritual, and physical components
at any level of health or illness, people can be
healthy or ill and still possess a high degree of
wellness.
At least among the better educated, the tradi-
tionally narrow view that equates health with
the absence of disease has already given way to a
broader, positive concept based on Greenberg’s
definition. In day-to-day terms, attainment and
maintenance of health are no longer just a mat-
ter of an annual medical checkup, but also
include engaging in regular exercise, making
sensible food choices, getting sufficient sleep,
having some form of spiritual belief, maintain-
ing friendships, and indulging in a diversity of
interests. Society is much less tolerant of destruc-
tive behaviors like smoking and drunken driv-
ing than it once was, and interest in healthy
eating has never been higher.
It is recognized, however, that this positive
view has not permeated all strata of society to
the same extent.33,95 There are good reasons
why. At the individual level, education results in
greater access to knowledge and information,
and it develops information-seeking attitudes
and skills. In addition, better-educated people
usually lead lives that give them more opportu-
nities to develop healthy lifestyles than do those
who have to spend more time and energy in just
making ends meet. At the community level, the
characteristics of the neighborhood and com-
munities in which people live and work have
become recognized as prime determinants of
health status.50,51
This concept of health promotion began
to take root during the 1970s and was much
influenced by a working paper put out by the
Canadian Minister for Health at the time, Marc
Lalonde. More of a visionary than many politi-
cal leaders, Lalonde introduced the health field
concept, a new idea at the time, as he tried to
evaluate the impact of Canadian health poli-
cies.57 Specifically, Canada had moved to a pro-
gram of equal access to health care for all
citizens through public financing, and Lalonde
had observed that increased access to health
care services did not by itself improve health
status.
The health field concept, as Lalonde envi-
sioned it, is a framework for the evaluation
and analysis of community health needs that
5 Oral Health Promotion 51
includes assessments of human biology, envi-
ronment, lifestyle, and health care organization
in more or less equal parts. Before Lalonde’s
analysis, such assessments had usually been
dominated by health care organizations (i.e.,
the view was that health services equal health),
but today we are much more aware of the
importance of the other factors as well. The
cohesion and functionality of a community is
often expressed as its social capital, which con-
sists of features of social organization such as
trust between citizens, norms of reciprocity, and
group membership, that facilitate collective
action.52 The wider concept of health promo-
tion includes the investment of social capital,
which can relate health status to availability
of community amenities such as libraries,
recreational facilities, biking and walking trails,
public transportation, and employment oppor-
tunities, things that are provided by the com-
munity rather than by the individual. Factors
that were seen by the influential Ottawa Charter
as fundamental preconditions for health are
shown in Box 5-1.
In an ideal world, governments would have
policies in place that do not interfere with peo-
ples’ lives but that give them the freedom to
make informed choices on their health behav-
ior. As a negative example, homeless people are
preoccupied with fundamentals of day-to-day
survival and live in a world that is deficient in
many of the preconditions for health listed in
Box 5-1. As a result, they have little opportunity
to make rational choices on matters affecting
their health. The first step in promoting health
among the homeless, therefore, is to provide
BOX 5-1 Fundamental Social Preconditions and
Resources for the Achievement of Health, as Defined
by the Ottawa Charter for Health Promotion101
●
Peace
●
Education
●
Shelter
●
Food
●
Income
●
A stable ecosystem
●
Sustainable resources
●
Social justice and equity
52 Dentistry and the Community
decent housing and adequate food, and do
whatever else can be done to improve self-
esteem. If we hark back to the definition of
health promotion, we see that such steps
represent the organizational, social-economic,
and environmental supports that are basic
to the development of healthy behaviors.
Governmental action in this area often means
legislation. In the high-income countries we are
familiar with specific laws on matters like ciga-
rette advertising, use of seatbelts and safety hel-
mets, and immunizations for children. These
laws, through which society accepts some con-
straints on absolute freedom in the interest of
public health, are in addition to the public
health codes covering water supplies, food
preparation, and public accommodations. In
the oral health area, legislation that mandates
or permits water fluoridation, and the statutory
basis in some countries for school dental pro-
grams, are both organizational aspects of oral
health promotion.
COMMUNITY-BASED HEALTH
PROMOTION
The principal community-based health promo-
tion programs that have been conducted in the
United States have been directed at reducing the
risk for cardiovascular disease. Nothing on this
scale has been carried out for oral health,
though there are issues in these programs from
which dentistry could well learn for implemen-
tation of its own health promotional programs.
Three major community-based programs
aimed at reducing the risk factors for cardiovas-
cular disease were implemented in the United
States during the 1980s. All were focused on
individual risk factors, because an appreciation
of the role of social factors was still in its infancy
at the time. These programs were conducted
in Pawtucket, Rhode Island,8 the state of
Minnesota,46 and five cities in central California.27
These projects were completed by the 1990s,
and in retrospect they were all modestly success-
ful, though not as conclusive as had been
hoped.2,28,35 Certainly a great deal was learned
about the benefits and limitations of large-scale
health promotion programs.
The projects had some features in common:
The extensive use of epidemiologic data in
●
planning. Specific data on the frequency of
heart attacks in the communities con-
cerned was added to research information
on the major risk factors: hypertension,
obesity, sedentary lifestyle, smoking, high-
fat diets, and high blood cholesterol levels.
●
Educational and interventional activities
were based on currently accepted theories
of health behavior.
●
Clearly specified hypotheses, involving
measurable exposures and outcomes,
could be readily tested to evaluate the suc-
cess of the projects.
To assess the impact of community-wide health
promotion, it is worth looking at one of these
projects in detail. The purpose of the Stanford
Five-Cities study, as an example, was to seek
reductions in the cardiovascular risk factors of
smoking behavior, high blood cholesterol level,
and hypertension. The project began as the
Stanford Three-Community study in 1972,23
and promising results led to its expansion to
become the Five-Cities study. The project was
designed to test whether a comprehensive pro-
gram of community organization and health
education would produce favorable changes in
risk factors, morbidity, and mortality in two
treatment cities compared to three control cities
over a period of 6 years. The methods chosen for
comparative study were mass media health edu-
cation in one city, and mass media education
plus personal instruction for those at highest
risk in the second.
This 6-year intervention was influenced by
Bandura’s social learning theory.4 This theory
states that reciprocal relationships exist between
an individual’s behavior, cognitive processes,
and the external environment, and that these
relationships are mediated by self-efficacy: the
individual’s belief in her competence to carry
out specific actions. In practical terms, this
theory states that the professional office envi-
ronment is not conducive to learning and main-
taining good health behavior; such activities are
best carried out at home, at work, and in other
community settings. The Stanford Five-Cities
study was a sophisticated program, making use
of community organization principles and
social marketing methods.
The Stanford study design included biennial
assessments of cohorts followed over the 6 years
and assessments of independent cross-sectional
samples at 2-year intervals. Results at the end of

the 6 years showed that the treatment cities
exhibited greater improvements with regard to
most of the risk factors being measured (cardio-
vascular disease knowledge, blood pressure,
smoking behavior, resting pulse) than the con-
trols.22,29 Mixed results were found for body
mass index,86 which suggests less than fully
effective results. What were not expected were
the improvements in the control cities, presum-
ably due to the widespread media publicity
given to cardiovascular risk factors.30 Although
findings overall were positive, the beneficial
trends in the control cities made the net changes
attributable to the program rather small.
A major question after such large-scale proj-
ects is whether the good results achieved are
maintained after the project’s completion. To
answer that question, participants in the
Stanford project were followed up 4 years after
the main project finished. Small net improve-
ments in most risk factors measured were main-
tained in the treatment cities relative to the
control cities, though trends in body mass index
went the wrong way in both treatment and con-
trol cities.97 This outcome was similar to the
one found in the Minnesota Heart Health
Program, in which strong efforts at obesity con-
trol ended in failure,49 and in Pawtucket, where
levels of physical exercise did not increase.19
The conclusion of the Stanford researchers was
that the modest net differences suggested that
new designs and forms of intervention are
needed to better reach those at highest risk.
Later reflections on the Stanford study in health
promotion included the rather humble admis-
sion that the researchers had learned little about
the factors which determine population-level
change, and the lowering of risk factors in the
control cities was clearly unexpected.27
When the combined success of the interven-
tions in all three of the cardiovascular health
promotion projects was assessed, trends were in
the favorable direction, although most differ-
ences between treatments and controls were not
statistically significant.64,96 There was agree-
ment, however, that the success of community
interventions of this type was linked to the com-
munity organization process.68
Cardiovascular disease is a life-and-death
matter, and the modest impact of these exten-
sive and expensive health promotional inter-
ventions on such a serious disease is sobering.
5 Oral Health Promotion 53
At the same time, most risk factors showed an
overall secular decline in both treatment and
control cities, which is good news. The conclu-
sion that we really don’t know much about how
to effect community-wide behavioral change
seems the correct one here. For dentistry, it is
worth reflecting on the lessons from these car-
diovascular studies, given that apart from
oral cancer we do not deal with life-threatening
diseases.
PROMOTION OF ORAL HEALTH
Health promotion requires active interventions
at different levels and by different organiza-
tions, and the health professional organizations
are certainly important components. Campaigns
conducted by professional organizations them-
selves, however, are often a mix of health pro-
motion and public relations. Public relations
exercises may have their place, but they should
not be confused with health promotion. The
American Dental Association (ADA), for exam-
ple, launched a television campaign in the
mid-1980s to increase patient visits among
adults over age 30 years, mostly by presenting
the health benefits of regular dental care.15
Although the ADA’s House of Delegates voted
not to finance this campaign nationally, several
state associations picked it up for local use. The
success of this campaign, in terms of improving
oral health, is uncertain because of its narrow
focus. The same could be said about an institu-
tion like National Children’s Dental Health
Month and special events in that month like
Give Kids a Smile! Day. The activities aimed at
getting dentists more involved in smoking ces-
sation among their patients (see Chapter 30),
although obviously focused on the individual
patient, are also a contribution toward commu-
nity health promotion.
Dentists and dental hygienists spend a lot of
time in educating their patients, and the public,
on the value of good oral health. Organized cam-
paigns such as the ADA’s Children’s Dental
Health Month have also been conducted fairly
regularly. All this effort has probably had some
impact, though we can’t tell just how much.
There is little question that over the last few
decades the status of the public’s oral health, and
its standards of oral hygiene, have continued to
improve. Once again, however, we do not know
54 Dentistry and the Community
how much of this can be attributed directly to
oral health education and how much to rising
living standards and norms of personal cleanli-
ness and grooming (i.e., the type of “external”
influences that were noted earlier in the Stanford
Five-City study: good things happening outside
of our control). We can also accept that the rising
utilization of dental services (see Chapter 2) is
evidence of increasing public acceptance of the
value of good oral health.
The mass media, especially television, are fre-
quently used in promotional programs in oral
health, but again the effects are hard to meas-
ure. For example, a national campaign in
Finland in the early 1980s used the mass media
to try to increase demand for dental services.
Although the proportion of adults making an
annual dental visit rose from 54% to 65%, the
researchers concluded that the mass media were
not effective in changing health behavior.69 The
value of the mass media in promoting dental
visits and good oral health behavior was also
questioned after a 1980s campaign in the
Netherlands.78 These findings were not really
surprising, because researchers earlier had
defined the limitations of mass media in chang-
ing health behavior.9,32 The Stanford Five-City
cardiovascular intervention program, described
earlier, also reached ambivalent conclusions on
intervention strategies that relied heavily on tel-
evision and newspapers.
One problem in defining a role for mass
media in oral health promotion is that evaluation
carried out by market researchers, accustomed to
dealing with commercial advertisements, is often
“process” evaluation that stops short of detecting
outcomes. An example is seen in the evaluation
of a Michigan television campaign in the late
1980s. Correct description of the advertisements
was given by 22% of a random sample of adults,
up from 13% early in the campaign. Aided recall,
meaning recall after some prompting, rose from
23% to 32%, and 12% of those interviewed said
they were influenced by the commercials.56
Recording whether the message was seen and
understood is relatively cheap and easy to do by
an experienced social research group, but measur-
ing the actual impact of the campaign on oral
health is more complicated.
An example of an oral health promotional
campaign is a sealant program conducted by the
Ohio Department of Health.82 Results of an oral
health survey of children in Columbus, which
showed that caries experience was greatest
among poorer children, were used as the ration-
ale for grant support, which permitted continua-
tion, and even expansion, of the sealant program
in the city schools. But the data served wider pur-
poses as well. They were invaluable in “market-
ing” the program among influential legislators,
in developing a supportive constituency among
parents and school personnel, and in educating
the public. The end result was a preventive pro-
gram that not only directly improved the oral
health of the children concerned but that had the
solid support of the community because its pur-
poses were well understood and accepted.
Oral health promotion is more encompass-
ing than dental health education and takes a
broader approach to closing the oral health gap
between the social strata. Oral health promo-
tional efforts today should include the common
risk factor approach, which brings oral health into
the health mainstream by recognizing that
much general health promotion (e.g., concern-
ing tobacco use, diet, and hygiene) is also related
to oral health.81 The role of social capital in oral
health promotion is still being worked out,
though some role for it is generally accepted.
The growth of interest in epidemiology across
the life course, which addresses the question of
how events and circumstances in childhood
affect health in adulthood,93 will also help give
oral health promotion a stronger scientific basis.
GOALS FOR ORAL HEALTH
At the international level, global goals for oral
health in the year 2000 were established by the
Fédération Dentaire Internationale (FDI, now
the World Dental Federation) in 1982 and are
listed in Box 5-2. These goals were developed
after a great deal of discussion and with the
strong involvement of WHO. They have passed
into history now but are shown because they
pretty well did what they were supposed to
do—that is, stimulate individual countries
either to adopt them as they are for their own
goals or to modify them to fit their own circum-
stances. The FDI followed up on these global
goals with its guidelines for national dental
associations to use in promoting the oral health
of the public.12 Unfortunately, new goals for the
new century have not been established.

BOX 5-2 Global Goals for Oral Health in the Year 2000, Established by the World Dental Federation and the
World Health Organization in 198224
●
50% of 5- to 6-year-olds will be caries-free.
●
The global average will be no more than three
decayed, missing, and filled teeth at age 12.
●
85% of the population will retain all their permanent
teeth at age 18.
●
A 50% reduction from present levels of
edentulousness at ages 35-40 years will be achieved.
The United States first adopted its own
national goals for health in 198088 as part of a
10-year plan for improvement of national
health status by 1990. A midcourse review91
found that some of the oral health goals in this
plan had already been achieved, others clearly
would not be achieved, and still others could
not be evaluated because of a lack of data. In the
process, it became clearer than ever that goals
were not going to be met without specific pro-
grams and that programs required funds and
trained personnel if they were to have any
impact. National goals for health for the year
2000 were announced in September 1990,89
with generally favorable media publicity.
Among them were 16 goals for oral health.
Midcourse reviews found that, despite some
progress, disparities were growing between
some minority groups and the main population
in some areas. As a result, new subobjectives
were established for Native Americans for
reduction of the number of edentulous persons
and for African-Americans for the prevention of
oropharyngeal cancer.90
The goals for the year 2010, known as Healthy
People 2010,87 included 467 health objectives
altogether. One could argue whether a much
smaller number of goals, perhaps a set that
could be easily recalled, might be more effec-
tive—it is hard to remember 467 objectives, and
it could be that the nation’s resources are spread
thin with that many. The purpose of the Healthy
People objectives is to give guidance to public
health departments in their choice of programs,
to guide the nation’s public health research
agenda. The 17 oral health objectives from
Healthy People are shown in Box 5-3. They are, of
course, not everything that could be listed in the
pursuit of oral health but are more of a consen-
5 Oral Health Promotion 55
●
A 25% reduction from present levels of
edentulousness at age 65 years and older will be
achieved.
●
A database will be established for monitoring changes
in oral health.
sus priority listing. Some baseline data are
presented for each objective (not shown in Box
5-3). These provide the point of reference
against which progress will be measured.
As just mentioned, however, goals without a
program to achieve them are little more than
wishful thinking. Plans to reach the Healthy
People 2010 goals require a high level of agree-
ment and coordination among federal,
state, and local agencies, and between public
and private sectors. Successful achievement
of most goals is unlikely without the allocation
of sufficient resources for the necessary
programs.
KNOWLEDGE AND ATTITUDES ABOUT
ORAL HEALTH
People demonstrate a wide variety of attitudes
toward teeth, dental care, and dentists. These
attitudes naturally reflect their own experiences,
cultural perceptions, familial beliefs, and other
life situations, and these attitudes strongly
influence oral health behavior.10,34,63,98,103
Negative attitudes toward oral health are a
strong factor in loss of teeth (see Chapter 19).
For example, it was found in the Netherlands
that the majority of decisions for full-mouth
extractions are made by the patient rather than
the dentist,7 and a Scottish study related total
tooth loss to negative attitudes about dental
care and passivity about tooth loss.70 It is possi-
ble that these negative attitudes might be
unconsciously encouraged by dental profes-
sionals if the patient does not fit the “good
patient” model. Not surprisingly, dentists’ pro-
file of a “good” patient was one who shared the
dentist’s values on oral health, complied
with advice and accepted treatment plans, was
56 Dentistry and the Community
BOX 5-3 Healthy People 2010 Objectives for Oral Health for the United States87
21-1. Reduce the proportion of children and
adolescents who have dental caries experience
in their primary or permanent teeth.
21-2. Reduce the proportion of children, adolescents,
and adults with untreated dental decay.
21-3. Increase the proportion of adults who have
never had a permanent tooth extracted because
of dental caries or periodontal disease.
21-4. Reduce the proportion of older adults who have
had all their natural teeth extracted.
21-5. Reduce periodontal disease.
21-6. Increase the proportion of oral and pharyngeal
cancers detected at the earliest stage.
21-7. Increase the proportion of adults who, in the past
12 months, report having had an examination to
detect oral and pharyngeal cancers.
21-8. Increase the proportion of children who have
received dental sealants on their molar
teeth.
21-9. Increase the proportion of the U.S. population
served by community water systems with
optimally fluoridated water.
21-10. Increase the proportion of children and adults
who use the oral health care system each
year.
concerned about oral health, arrived on time,
and paid the bills.72 Because the same study
found that “personal warmth” in a patient was
valued by dentists, it is likely that many dentists
have trouble in warming to patients who do not
possess these attributes.
Knowledge gaps concerning a number of pre-
ventive procedures have been found between
researchers, practitioners, and patients,71 and
lack of consensus between researchers and prac-
titioners has been identified as a major barrier
to more effective promotion of caries preven-
tion. This unfortunate confusion can be allevi-
ated by health promotional activities aimed at
changing attitudes and practices. For example,
dentists in one Indian Health Service region
developed a significantly greater orientation
toward preventive services after such a promo-
tional campaign.62 With the realization that
positive attitudes toward health promotion
need to be developed during student days rather
than afterward, the FDI has recommended that
21-11. Increase the proportion of long-term care residents
who use the oral health care system each year.
21-12. Increase the proportion of low-income children
and adolescents who received any preventive
dental service during the past year.
21-13. Increase the proportion of school-based health
centers with an oral health component.
21-14. Increase the proportion of local health departments
and community-based health centers, including
community, migrant, and homeless health centers,
that have an oral health component.
21-15. Increase the number of states and the District of
Columbia that have a system for recording and
referring infants and children with cleft lips, cleft
palates, and other craniofacial anomalies to
craniofacial anomaly rehabilitative teams.
21-16. Increase the number of states and the District of
Columbia that have an oral and craniofacial
health surveillance system.
21-17. Increase the number of tribal, state (including
the District of Columbia) and local health
agencies that serve jurisdictions of 250,000 or
more persons that have in place an effective
public health dental program directed by a
dental professional with public health training.
substantial changes in the dental curriculum be
implemented to give dentists the knowledge,
skills, and attitudes they will need.25 The behav-
ioral sciences, and the control of fear and anxi-
ety in patients, were listed among those areas
needing more attention. Knowledge and atti-
tudes on oral health among other influential
professionals—schoolteachers, for example—
also can be disappointingly poor,37,58,61 which
only underlines the responsibility of the dental
professions to see that trainee teachers, nurses,
and others who influence public attitudes
receive correct information on oral health.
Even a relatively low level of serious oral dis-
ease in the community does not always reflect
positive dental attitudes. In fluoridated Hong
Kong, for example, where neither caries nor
periodontitis were found to be major public
health problems, ignorance and misconcep-
tions about the most common oral conditions
were widespread.60 Poor knowledge of the oral
diseases is common in many countries, includ-

ing the United States and Canada, as shown by
reports that many people do not associate exist-
ing symptoms, such as calculus deposits or
bleeding gums, with periodontal diseases.36,59
A more encouraging study in North Carolina
found that patients of general practitioners
were generally knowledgeable about the signs,
causes, prevention, and treatment of periodon-
tal conditions.3 Few serious misconceptions
were found in this study, though improvement
was needed on the significance of bleeding
gums. When incipient disease cannot be recog-
nized, there will naturally be inadequate self-
care, and promotion of self-care is one of the
major goals of oral health education.
DENTAL HEALTH EDUCATION
In the past, unless health professionals were
unusually sensitive to patients’ reactions, health
education often had a patronizing ring to it.
When a health provider who believes she knows
what is best for the patient “educates” a person
who is tacitly assumed to know nothing, it is a
safe bet that little of value eventuates. This has
been called the “empty vessel” approach to
health education: the patient is empty and wait-
ing for the health professional to “pour in” the
knowledge. This approach was enshrined in an
early WHO report,99 which saw the need to
teach educational theory and methods to stu-
dent dentists so that they could successfully
“motivate” their patients and the public to
behave as dentists would like them to. It also
shows itself unconsciously in terminology
such as toothbrushing drills, a so-called educa-
tional method in which children are taught
to brush their teeth in a semimilitary manner.
The empty vessel approach also dated from a
time when the guild model of professionalism
(see Chapter 1) was accepted, a model that saw
the all-knowing professional as dominant in
dentist-patient relations.
In more recent years, greater acceptance has
been given to the idea that the recipients of all
this attention might have some thoughts of
their own. Item 4 in the Declaration of Alma-
Ata, the outcome of a major international con-
ference on primary health care, stated that
“people have a right and duty to participate
individually and collectively in the planning
and implementation of their health care.”100 In
5 Oral Health Promotion 57
a subsequent WHO report, the evolution of pro-
fessional attitudes was demonstrated when it
was stated that (1) participant involvement was
essential for success in health education, and
(2) what is taught needed to be compatible with
local customs and culture as well as with scien-
tific knowledge.102
It is a basic precept that everyone has a right
to the best available knowledge about caring for
her own health. However, knowledge alone
does not lead to action. Many health care work-
ers can labor under the assumption that when
people have knowledge about health care they
will act upon that knowledge. It is a rational
assumption, but human behavior is more com-
plicated than that. Knowledge dissemination is
a fundamental part of the mission of health
professionals, but health care workers have to
steel themselves to accept that much of their
effort will go unheeded.
School-based oral health education pro-
grams, by definition, are aimed at more cohe-
sive groups rather than at the public at large.
Whatever approach is to be adopted, it will
require a plan of action, with appropriate
involvement of all parties concerned and clear
delineation of responsibilities. Fundamental
components of a school-based program for the
promotion of oral health have been described
as follows:
●
Oral health services, meaning preventive
procedures, health screening and treat-
ment, referral, and follow-up.
●
Health instruction, to include both per-
sonal and community health topics.
●
A healthy environment, with attention to
all aspects of the school environment that
could affect the health of students or
school personnel.45
Even though schoolchildren are more homoge-
neous than the public as a whole, any group of
them still has a variety of beliefs and attitudes;
in a multicultural society the differences can be
profound.18 Methods used in school programs
should therefore be a mix of small group and
mass approaches, and some are clearly more
successful than others. The more successful
approaches, as shown by evaluations of teachers
and administrators, and by the oral health of
participants, use a fair degree of active involve-
ment.13,14,26,43,73,80,84 This finding applies to all
ages and social groups, for active involvement
58 Dentistry and the Community
increased the effectiveness of programs con-
ducted with employed adults42,75 and with
mothers of young children.44 Nursing home
residents who monitored their own progress
toward oral hygiene goals showed improve-
ments in psychological well-being and self-
esteem as well as in oral hygiene.54,55
On the other hand, programs that involve
less individual participation can increase
knowledge of oral disease mechanisms and its
prevention but have less impact on attitudes,
beliefs, and behavior.60,76,92 The mass media,
which by definition do not develop personal
involvement, are generally seen as effective in
disseminating basic knowledge, but whether
they do much to influence behavioral change is
uncertain. We have learned from public oral
health campaigns that personal involvement
is needed to effect behavioral change. When the
cultural competence needed to accommodate
to the astonishing cultural variety in modern-
day America is added in, designing programs
for personal involvement becomes a challenge.
The most intensive form of oral health edu-
cation is one-to-one instruction. Although oral
health education is clearly an integral part of
professional responsibility, simply passing
across information does not by itself lead to
desirable action; personal involvement (again)
is necessary. A study of educational outcomes
among “high-plaque” patients who received
instruction in oral hygiene in dental practices in
Washington found that only 28% substantially
reduced their plaque scores over 6 weeks, and
BOX 5-4 Principles of Oral Health Education
●
People interpret health messages through the filter of
their own values, beliefs, and attitudes. These need to
be understood as far as possible, if the educational
process is to have any chance of success.
●
The most successful education maximizes self-
involvement of the participants.
●
Mass media are effective in transmitting simple and
consistent messages, although their value in
influencing health behavior seems limited. They have
been found effective in accomplishing some
behavioral change related to cardiovascular disease,
in 13% scores actually got worse. The researchers
concluded that the therapists often did not fol-
low the principles of effective instruction,
though outcomes were also related to patients’
oral status and life situations.94 The same study
also found that educational effort was not being
concentrated on those patients with greatest
need but rather was more or less equally distrib-
uted.67 A British project found that use of the
Community Periodontal Index of Treatment
Needs (as it was then named, see Chapter 16)
was a useful way of improving patient aware-
ness of periodontal conditions.11
Many health care professionals have enor-
mous faith in the value of dental health educa-
tion. Educational programs are rarely opposed
on the grounds that the resources involved
might better be placed elsewhere, and educa-
tional programs promote a general “feel-good”
atmosphere among all concerned. There is no
question that all people have a right to the best
knowledge about how to care for their health,
even though they will act on this knowledge in
different ways. The conclusions from a search-
ing review of dental health education outcomes
should be borne in mind by all those planning
educational programs: (1) educational pro-
grams work well in improving knowledge lev-
els; (2) they have a positive but temporary effect
on plaque levels; and (3) they have no dis-
cernible effect on caries experience.53
At a practical level, the principles of oral
health education that emerge from the litera-
ture can be summarized as shown in Box 5-4.
but have been less effective in producing change in
relation to oral conditions.
●
Health professionals have to accept that not all people
share their values about the importance of health. An
acceptance of all components of wellness, not just
physical health, will help in dealing with the infinite
variety of human beliefs on health.
●
Dental health education programs can improve
knowledge and temporarily improve oral hygiene but
have not demonstrated any direct effect on caries
experience.

PROMOTION OF WATER
FLUORIDATION
Water fluoridation is an issue that gives dental
professionals the chance to promote oral health
at the community level and to apply the experi-
ences gained from other successful community-
based campaigns. The ADA has a long-standing
policy that dentists should work to promote
fluoridation in their communities,1 though it is
recognized that the issue can provoke mixed
feelings. Dentists and hygienists, accustomed to
life outside the spotlight, are often far from
comfortable in the public arena. For such indi-
viduals, there are still key roles for dental pro-
fessionals as low-profile resource persons.
To begin with, dentists and hygienists should
at least educate their patients about what fluori-
dation is and who benefits from it (see Chapter
25). They should actively persuade patients to
vote for the measure if a referendum is coming.
Patients, after all, are a more or less captive
audience, and there is evidence that dentists
could do better with this particular educational
role.48 Dental professionals should know the
concentration of fluoride in their own commu-
nity’s drinking water, information that comes
from the state or local health department. Cost
estimates for fluoridating a community’s water
can be obtained from the state health depart-
ment or water supply division, and from the
fluoridation engineers at the Division of Oral
Health of the Centers for Disease Control and
Prevention (CDC) in Atlanta, Georgia. If there
were previous attempts to fluoridate the com-
munity, it helps to have a history of which indi-
viduals were involved and what happened.
At the local community level, a decision by a
city council to fluoridate has proven far more
likely to result in a favorable outcome than a
referendum. Lobbying of city councilors both
answers questions and identifies the members
who are for, against, and undecided, informa-
tion that can then help shape the further pro-
motional effort needed. When a city council
decides to put fluoridation out for referendum,
the role of dental professionals becomes more
overtly political. Defining this role may not be
easy. A thoughtful study in the 1960s, still rele-
vant today, found that political efforts of den-
tists and other health professionals in a local
fluoridation campaign got unfavorable reac-
5 Oral Health Promotion 59
tions for two different reasons.77 First, the com-
munity expected partisans in a political cam-
paign to be motivated by self-interest and to
conduct a propaganda campaign to further
those interests. Because the health professionals
supporting fluoridation were seen as political
partisans, their endorsements of fluoridation
were not accepted as dispassionate expert testi-
mony. Second, their efforts to maintain profes-
sional decorum and to avoid the hurly-burly of
open controversy were interpreted as arrogance.
This study suggests that, in a fluoridation refer-
endum, the health professionals cannot expect
to maintain a detached role, and referendum
tactics must be structured accordingly.
Regardless of the nature of the political cam-
paign, experience has shown that a successful
outcome is more likely when the campaign is
coordinated by a citizens’ committee, often
called Citizens for Healthy Teeth or some such
name. The first task of the coordinating com-
mittee is to draw up a plan of action that will
guide the promotional activities. Dental profes-
sionals can play the role of technical experts in
this committee, though many have the qualities
to take more prominent roles. If needed, the
CDC and the ADA have materials to help. The
composition of the citizens’ committee should
be as broadly based as possible, with attention
to socioeconomic, age, and ethnic groupings, in
order to accomplish the following:
●
Represent the community and demonstrate
that fluoridation has widespread political
support.
●
Increase the number of volunteer workers
for telephoning potential voters, canvass-
ing, and distributing materials.65
●
Increase the base of financial support.47
Experience has also shown that a hired consult-
ant in political organization can be very help-
ful.21 A political expert can assist in these areas:
●
Legal registration of the political action
committee in those states in which it is
required
●
Outreach to the large segments of the pop-
ulation that ordinarily do not participate in
organizations and are not much influenced
by mass media
●
Identification of the community power
structure and the key individual leaders
whose support will be needed.
●
Campaign strategy and tactics
60 Dentistry and the Community
Recruitment of “celebrities” and “outside
● 6. Boriskin JM, Fine JI. Fluoridation election victory:
experts,” should it be decided to use them
The political tactics used vary with each com-
munity. There is no cookbook, although there
are some standard issues. For example, should
an invitation to publicly debate a fluoridation
opponent be accepted? There is no easy answer.
A refusal can be interpreted as professional arro-
gance, but at the same time a debate with a
committed opponent cannot be “won.” An
opponent can imply, for example, that fluorida-
tion is in the same category as toxic chemical
waste or acid rain, and that proponents are try-
ing to increase both unnecessary regulation and
taxes. Despite the successful record of fluorida-
tion in the courts (see Chapter 25), a good
speaker can still score on the freedom-of-choice
issue. Even the necessary dissemination of
objective facts on fluoridation can be self-
defeating, for the burden of proof always falls
on those advocating change. Skilled opponents
of fluoridation can quickly throw the propo-
nents onto the defensive.
Successful referendum campaigns have
been reported in the dental literature, and
strategies for dealing with fluoridation in
the political arena have now been well
defined.6,16,17,20,21,47,74,79 The common theme
in these reports is that fluoridation is politics. It
demands the use of the media, publicity, educa-
tion, intensive door-to-door canvassing, tele-
phone campaigns, and getting out the vote on
polling day. Above all, it means consistent hard
work over a long period and starting with a
solid preparation.
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63. McCaul KD, Glasgow RE, Gustafson C. Predicting levels
of preventive dental behaviors. J Am Dent Assoc
1985;111:601-5.
64. McGovern PG, Jacobs DR Jr, Shahar E, et al. Trends in
acute coronary heart disease mortality, morbidity, and
62 Dentistry and the Community
medical care from 1985 through 1997: The Minnesota
heart survey. Circulation 2001;104;19-24.
65. McGuire KM. Strategies for a fluoridation campaign.
J Mich Dent Assoc 1981;63:681-6.
66. McGuire MK, Sydney SB, Zink FJ, et al. Evaluation of an
oral disease control program administered to a clinic
population at a suburban dental school. J Periodontol
1980;51:607-13.
67. Milgrom P, Weinstein P, Melnick S, et al. Oral hygiene
instruction and health risk assessment in dental prac-
tice. J Public Health Dent 1989;49:24-31.
68. Mittelmark MB, Hunt MK, Heath GW, Schmid TL.
Realistic outcomes: Lessons from community-based
research and demonstration programs for the preven-
tion of cardiovascular diseases. J Public Health Policy
1993;14:437-62.
69. Murtomaa H, Masalin K. Effects of a national dental
health campaign in Finland. Acta Odontol Scand
1984;42:297-303.
70. Nuttall NM. Characteristics of dentally successful and
dentally unsuccessful adults. Community Dent Oral
Epidemiol 1984;12:208-12.
71. O’Neill HW. Opinion study comparing attitudes about
dental health. J Am Dent Assoc 1984;109:910-5.
72. O’Shea RM, Corah NL, Ayer WA. Dentists’ perceptions
of the “good” adult patient: An exploratory study. J Am
Dent Assoc 1983;106:813-6.
73. Olsen CB, Brown DF, Wright FA. Dental health promo-
tion in a group of children at high risk to dental disease.
Community Dent Oral Epidemiol 1986;14:302-5.
74. Paul BD. Fluoridation and the social scientist: A review.
J Soc Issues 1961;17:1-12.
75. Petersen PE. Evaluation of a dental preventive program
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Epidemiol 1989;17:53-9.
76. Peterson FL Jr, Rubinson L. An evaluation of the effects
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education program on the knowledge, attitudes and
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Health 1982;52:63-9.
77. Raulet HM. The health professional and the fluorida-
tion issue: A case of role conflict. J Soc Issues
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78. Reelick NF, Verbeek MH. The Dutch dental campaign.
J Am Dent Assoc 1986;113:803-4.
79. Rosenthal DB, Crain RL. Executive leadership and com-
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80. Schou L. Active-involvement principle in dental health
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81. Sheiham A, Watt RG. The common risk factor
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399-406.
82. Siegal MD, Martin B, Kuthy RA. Usefulness of a local
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83. Simons-Morton BG, Greene WH, Gottlieb NH.
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84. Sogaard AJ, Holst D. The effect of different school
based dental health education programmes in
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85. Sogaard AJ, Koch AL. Dental health education—
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 6 The Practice of Dentistry
PRIVATE DENTAL PRACTICE
Solo Practice
Group Practice
Franchised Practices and Department Store
Clinics
HOSPITAL DENTISTRY
PUBLIC PROGRAMS
Auxiliaries in Public Programs
Primary Health Care
Organized dentistry has two primary goals: to
promote the oral health of the public and to
preserve the autonomy and economic well-
being of the profession. These goals can be in
conflict, however, when dentistry’s efforts to
secure its own well-being are perceived as not
being in harmony with the public interest, or
when public efforts to improve oral health are
seen by the professions as antagonistic to their
self-interest. This type of conflict will continue,
with just and acceptable outcomes more likely
if the dental professions understand the pres-
sures that produce them.
A delivery system is a collective health care
expression that incorporates the various means
by which care is provided to patients. The prin-
cipal components are as follows:
●
The structure of the system, that is, the
organizational arrangements by which
patients meet up with providers.
●
The means by which the care is paid for.
●
The supply of various types of health care
personnel.
Other elements of a delivery system can be
identified, such as physical facilities and record
keeping, but the three elements listed here are
the most basic. They are interdependent; a
change in any one affects the others, although
this book divides the subject into three chapters
to give these issues adequate consideration.
QUALITY ASSURANCE
Evolution of Quality Assurance
Recent Emphasis in Quality Assurance
Examples of Quality Assurance Activities:The
Dimensions of Quality
Quality Assurance and Cost Control
This chapter examines the structure of dental
care provision systems in the United States, with
some reference to methods used elsewhere.
PRIVATE DENTAL PRACTICE
Traditionally dental care in the United States has
been delivered by independent private prac-
titioners. The American Dental Association
(ADA) estimated that approximately 93% of
all active dentists were in private practice in
1998.15 This proportion has remained remark-
ably stable over the years. Indeed, an essential
feature of dental care delivery in the United
States is the diversity of practice modes and their
constant evolution within a private practice phi-
losophy. Adaptability in a rapidly changing
world is a major strength of private practice, an
attribute that ensures that private practice will
endure.
Private practice has a number of inherently
desirable features. One advantage to both
provider and patient is flexibility. Dental practi-
tioners can provide care for as many hours per
day and for as many days per year as they
choose. When demand for care in a locality
increases, private practitioners can respond if
they wish by working longer hours, by increas-
ing their productivity to meet it, by increasing
their fees, or by all of these. There is a built-in
67
68 Dental Practice
economic incentive to be as efficient as possible
in private practice, because it represents a big
investment of private capital in facilities and
equipment; the return on that investment is the
practitioner’s profit. Choice of equipment,
materials, and employees therefore is made
carefully, and all can be chosen to suit the tastes
of the individual dentist.
Private practice has often been equated with
free choice of a dentist by the prospective
patient and, conversely, with freedom of the
dentist to treat or not to treat anyone seeking
care. Whether these concepts were ever fully
true is arguable, but it is certain that current
circumstances put some limits on these free-
doms. In many inner city or small rural com-
munities, for example, there is often little
choice of dentist because dentists are less likely
to establish practices there. Because dentists in
private practice are self-employed business
people, they tend to establish their practices in
localities where they can be reasonably sure of
adequate demand for their services; these
localities are typically higher-income subur-
ban areas. There is a clear association between
the availability of dentists and the per capita
income of an area.7,8,14 Fig. 6-1 shows this
association at the level of the states. Usually
there are relatively more dentists in states with
higher per capita incomes. This same phenom-
enon also is likely to apply to smaller geo-
90
80
Dentists per 100,000 population
70
60
50
40
30
20
10
0
0 10,000
Per Capita Income in Dollars
Fig. 6-1 The association between mean per capita income and the dentist/population ratio for individual states in
the United States, 2000.65,67
graphic units such as counties, cities, and other
natural market areas.
Even within communities that are well
stocked with dentists, some groups are not read-
ily treated in private practice (see Chapter 9).
Treatment of the preschool child with behav-
ioral difficulties, for example, requires a degree
of time, patience, experience, and training that
can make such treatment uneconomical for
many general practitioners to provide, and
pediatric dental specialists are not always avail-
able. Many elderly people cannot afford the care
that they need, and many have difficulty travel-
ing because of physical infirmities. In addition,
there are people who are chronically ill, men-
tally retarded, or physically challenged, or who
have illnesses that require them to receive den-
tal treatment in a hospital. Private practices that
are optimally designed for ambulatory, highly
compliant patients are often not well suited to
care for such persons.
Low-income individuals often have a double
problem: care is less available near where they
live, and when it can be found it is relatively
expensive. It is hardly surprising that people in
low socioeconomic areas are often thought “not
to value dental care.” That belief is not necessar-
ily true; rather, the circumstances of their lives
do not always permit the disadvantaged the lux-
ury of “valuing dental care” the way that den-
tists would like.30 Given this situation, “free
20,000 30,000 40,000 50,000

choice” can be most accurately described as a
middle-class value that may mean little in other
socioeconomic contexts.
Free choice also cuts the other way: dentists
have some freedom to reject patients (although
not solely on the basis of race, ethnicity, or
human immunodeficiency virus status; see
Chapters 3 and 10). Some practitioners may
believe that they are treating as many patients as
they can manage and therefore will accept no
new patients of any kind. Others may reject
patients whose care is financed by public pro-
grams such as Medicaid (see Chapter 7). This
rejection may be based on the dentist’s view
that such programs offer poor compensation
and are bureaucratic nightmares, or the dentist
may be unable to accept the attitudes and values
of low-income individuals.
From the community viewpoint, the princi-
pal advantages and disadvantages of private
practice as a delivery system relate to econom-
ics. Private funds are used to build the facilities,
buy equipment, hire auxiliary staff, and pay for
some of the expenses (although by no means
all; see Chapter 8) of dental education. Dentists
set their own fees. Dentists also have tradition-
ally practiced price discrimination, meaning that
they have charged wealthy patients higher fees
than they have charged poorer ones. Wealthier
patients in these practices therefore subsidized
the poorer ones.
The business demands of running a dental
practice can conflict with the need to provide
for the dental treatment of all people. Dental
fees simply are too high for some. The solo den-
tal practitioner has certain overhead costs to
meet: utilities, rent, equipment, supplies, staff
payroll, and insurance. These expenses must be
met regardless of whether or not patients come
and whether or not fees are collected. In addi-
tion, the dentist is a highly trained and qualified
professional and thus is deemed by American
culture to be entitled to a good income. Many
dentists graduate from dental school heavily in
debt because of the high costs of their education
and thus have a strong incentive to begin show-
ing profits soon after they begin practice. The
average debt among all dental graduates in
2003 was $118,750.17 It is interesting to com-
pare these facts of the dental practitioner’s posi-
tion with those of the position of the medical
surgeon, who does not have to pay for hospital
6 The Practice of Dentistry 69
beds and hospital support staff out of the
physician’s fee.
Solo Practice
Within the overall realm of private practice,
which is the principal form of dental practice in
the United States, the solo practitioner is the
most common form of practice. The ADA esti-
mated that in 1998 almost two thirds (65%) of
private practitioners worked in a practice with
no other dentists, about 20.5% worked with
one other dentist, and just over 14.5% worked
with two or more other dentists.16 This distribu-
tion is shown in Fig. 6-2.
Group Practice
The arrangements by which dentists can work
together are so varied that the term group practice
is difficult to define precisely. In fact, the ADA
has adopted the term nonsolo practice. The ADA
definition states the following:
A nonsolo dentist works in a practice with at least one other
dentist. Some of these dentists may be employed by the
owner dentist in the practice.3
As demonstrated in Fig. 6-2, solo practice
remains the most common form of dental prac-
tice, and nonsolo practices generally are small,
most of them consisting of two dentists.
Although it is uncommon for newly graduating
dentists to directly enter practice as a solo prac-
titioner, the long-term pattern suggests that the
dominance of solo and small group practices
will continue, with a possible gradual shift
toward small group practices.
One dentist
Two dentists
Three or more
dentists
Fig. 6-2 Distribution of private practitioner dentists by type
of practice in the United States, 1998.16
70 Dental Practice
Franchised Practices and Department
Store Clinics
In the late 1970s, several major department store
chains, including Sears and Montgomery Ward,
opened dental clinics in some of their stores and
announced their intention to open more. These
clinics operated during usual store hours, and
the stores’ management viewed them as an extra
service for their customers, no different from the
pharmacies and optical departments. However,
dental practices in department stores have not
prospered and were few in number by the
late 1990s.
The concept of franchises is common in the
United States, encompassing such varied entities
as motels, restaurants, automobile servicing,
retail stores, and child care services. The fran-
chisor, for some combination of initial fees and
periodic payments, provides the name plus addi-
tional services such as advertising, training, co-
ordinated purchasing, and management services.
The franchisee runs the individual business loca-
tion and, except for the agreed payments to the
franchisor, retains the profits from the business.
By the early 1980s, there appeared to be the
beginning of an explosive growth of franchised
dental practices.9,18,71 The idea as applied
to dental practice varied in detail among fran-
chises but tended to include such things as a
franchise name; marketing and management
services; bulk purchasing of supplies; and some-
times the design, construction, and equipping
of the practice itself. The dental clinic space was
usually leased by a dentist, because many state
laws do not allow dental practices to be owned
by a nondentist.
After a quick start in the early 1980s, most
franchise dental organizations had fallen on
difficult times by 1988;73 all but a few were out
of business or under bankruptcy protection.
Reasons for this turn of events include under-
capitalization, overexpansion, poor manage-
ment control, unprofessional image, and high
costs.73 Fundamental conflicts between the tra-
ditional strengths of franchises and dental prac-
tice make it unlikely that franchised dental
practice will ever be a major force. The standard-
ization of process and procedures that leads to
cost savings and uniform quality in many busi-
nesses is unlikely to produce cost savings in
dental care.
In the mid-1990s, there were a few reports of
dental insurers’ buying individual dental
offices. The reason for these purchases is usually
to acquire the capacity to handle managed care
offerings, particularly in areas where individual
dental offices are reluctant to sign on. The
impact of these arrangements will take some
years to be properly evaluated.
HOSPITAL DENTISTRY
Although only a small fraction of dental care is
provided in hospitals, dentists still have a sub-
stantial role in hospitals. In the mid-1980s,
approximately 1000 hospitals in the United
States had formally organized departments
of dentistry, and about 40,000 dentists were
members of the medical staff of at least one hos-
pital.10,33 In 1995, the number of dentists in the
United States with hospital privileges was still
about 40,000.13
The number of dental general practice resi-
dencies in hospitals grew rapidly through the
1970s, and as of 2003 there were 1423 first-
year hospital-based residency positions.17 The
extended experience in the hospital environ-
ment that these residencies provide is likely to
make it easier for these dentists to make use of
hospital privileges later in their careers. Many
dentists affiliated with these and other educa-
tional programs in hospitals have full-time or
substantial part-time commitments to hospital-
based care. Dentists in the military and with the
Department of Veterans Affairs are also com-
monly in hospital-based practices. The majority
of dentists who have hospital privileges, how-
ever, are in private practice and provide care
only occasionally in the hospital.
Dental care provided in hospitals is for those
situations in which general anesthesia and
other resources of a hospital are required, such
as for treatment of very young children with
rampant caries, oral surgery to remove carcino-
mas, cleft palate repair, and maxillofacial pros-
thetic treatment for victims of burns or trauma.
In addition, some routine dental care is pro-
vided in hospitals for patients who are suffering
from serious systemic disease and for whom the
risk of being treated in the private dental office
would be unacceptably high. The inclusion of
ADA representation on the board of the Joint
Commission on Accreditation of Healthcare

Organizations since 1980 helps to ensure an
appropriate role for dental consultation and
services within hospitals.
Beyond the traditional role of educational
programs and consultative services, a major
challenge for hospital dental departments is
economic justification. All departments within
hospitals are increasingly being pressed to show
that the income they produce is sufficient to jus-
tify their existence, and the traditional roles of
teaching, consultation, and care for indigent
patients do not provide high levels of revenue.
On the other hand, moves by hospital-based
programs to solicit insured patients through
ambulatory care facilities are seen as unfair
competition by some private practitioners.35,57
PUBLIC PROGRAMS
As stated earlier, private practice cannot meet
the dental demands of all people. A number of
public dental care programs therefore have
been developed to meet the needs of specific
groups. Some of these government-sponsored
programs use a specific delivery system in addi-
tion to a funding mechanism. Many receive
funding from the federal government, although
most still remain under the control of state and
local health departments. Many are under con-
siderable strain because social services budgets,
on which these programs heavily depend, have
been severely cut over recent decades.
The oldest health care programs of the fed-
eral government are directed either at certain
groups of its own employees or at other specific
groups for whom it has an obligation or who
would find it difficult to get care anywhere else.
Each branch of the armed forces, for example,
provides dental care for its own active-duty per-
sonnel. Care is provided for the most part by
dentists who themselves are members of the
armed services and is dispensed from clinical
facilities wholly owned and maintained by the
service concerned.
Many of the long-established clinical programs
of the U.S. Public Health Service were described
in Chapter 1. In addition, the Community and
Migrant Health program of the U.S. Public
Health Service provides grants to support pub-
lic and nonprofit organizations to plan, develop,
and operate health care facilities, known as com-
munity and migrant health centers, in rural and
6 The Practice of Dentistry 71
urban areas where existing health care resources
are inadequate. These centers are primarily med-
ical, but many provide dental services too. As
of 2002 there were 1230 full-time-equivalent
(FTE) dentists, 383 FTE dental hygienists, and
2291 FTE dental assistants, aides, and technicians
employed at these health centers.66 These centers
are established in areas where access to private
care is limited, and they employ salaried dental
personnel.
Another program aimed at making care avail-
able in areas unattractive to private practice is
the National Health Service Corps. This pro-
gram, discussed more fully in Chapter 8, has
provided incentives, including scholarships and
loan repayment, to encourage dentists to prac-
tice in remote and underserved areas. Many
National Health Service Corps dentists practice
in community and migrant health centers.
Many states, counties, and cities have had
their own dental care programs, with their own
facilities and salaried personnel, operating for
years. Most of these programs, which are often
administered by an agency of the state or local
government, have been aimed at providing care
for people who are eligible to receive some form
of public assistance. The services available
through these programs vary widely. Many of
these state and local dental treatment programs
cover a portion of their costs of operation by
billing Medicaid for eligible patients and by
receiving Community and Migrant Health
program grants from the Bureau of Primary
Health Care.
Auxiliaries in Public Programs
Auxiliary-based programs have long been the
backbone of public dental care in some coun-
tries, although not in the United States. The old-
est and best known is the New Zealand school
dental nurse plan, introduced in 1921. New
Zealand is a nation of some 4 million people in
the South Pacific, 1500 miles off the eastern
coast of Australia. Living standards are high,
and New Zealand has been a world leader in a
number of social programs: old-age pensions,
visiting maternal and child health nurses, and
the secret ballot at political elections. A number
of these programs began in the late nineteenth
century, about the time that social security pro-
grams were initiated in Bismarck’s Germany.
Given these traditions, the introduction of the
72 Dental Practice
school dental nurse plan was not as radical an
innovation as it might seem, although there was
some concern among dentists at the time.61 The
stimuli for the program were the extensive den-
tal disease found in army recruits during World
War I (1914-18) and government intent to do
something about this problem. Dentists were in
short supply at the time, and treatment of
young children was not as accepted in dental
practice as it is now. Caries experience remained
high for a long time in New Zealand22,23 before
that country joined in the worldwide decline in
the late twentieth century (see Chapter 20).
When the service began, care was offered only
to younger school-aged children, but eligibility
was soon extended to all preschool-aged chil-
dren and all children in primary and intermedi-
ate school. Although most care is provided by
dental therapists (the current name for dental
nurses), recent legislation will extend practice
possibilities for dental therapists, including treat-
ing publicly funded clients in private practice
and treating indigenous populations.41 The tra-
ditional 2-year diploma program has also been
supplemented with a 3-year degree program.64
The therapist’s training concentrates on tech-
nical procedures, with considerable emphasis
on learning to recognize conditions that are
beyond the therapist’s competence to treat.
Individuals with these conditions are then
referred to a private practitioner or to one of a
small number of dentists employed by the
School Dental Service. Therapists’ clinical duties
include performance of oral examinations, cav-
ity preparation and placement of restorations,
pulp capping, and extraction of primary teeth.
Therapists also provide extensive dental health
education, both in the classroom and to indi-
vidual patients.
Dental therapists function with a high degree
of independence. Many young children in New
Zealand are examined and treated completely
by dental nurses and never see a dentist until
their teenage years. Although this fact has dis-
turbed some American observers,36,55 there is
no evidence that the oral or general health of
the children suffers as a result.
The decline in caries experience in New
Zealand, as in most developed countries, has
reduced the need for restorative treatment. In
addition, women are staying in the workforce
longer than they used to. As a result of these
influences, the intake of new trainees had to be
reduced. However, with many dental therapists
approaching retirement age, there is concern
that there may be a shortage in coming years.
The New Zealand school dental therapist
plan has attracted the attention of dental organ-
izations all over the world. Other countries
and jurisdictions that have adopted similar
programs, with modifications to suit the lo-
cal environment, include Canada, Great Brit-
ain, Australia, Thailand, Malaysia, Singapore,
Myanmar, Sri Lanka, Brunei, Hong Kong, and
Indonesia. A small number of dental health aides
are currently being trained in New Zealand to
prepare for practice under Alaska’s Community
Health Aide Program that serves native popula-
tions in Alaska.63
The few attempts to introduce dental thera-
pists in the United States have gone nowhere, at
least partly because of the consistently strong
opposition of the ADA.11,12 An attempt to intro-
duce an auxiliary-based school dental program
in Massachusetts in the mid-1950s was defeated
after political action by organized dentistry.31
Despite this history, it is well established from
research, much of it ironically conducted in the
United States, that well-trained dental thera-
pists are able to carry out many procedures as
well as dentists can.1,2,21,37,44–46,56,59 In most of
the countries where these programs are estab-
lished, children likely would be receiving no
care at all were it not for the dental therapists.
Primary Health Care
Developing countries generally do not have the
resources to train the number of dentists they
need. Even if large numbers of dentists were
available, the cost of care would still be beyond
the reach of most. Recognition of this fact has
led the World Health Organization to establish
its principles of primary health care.72 Under
this concept, the focus of health care is to assist
in maintaining health rather than to wait for
problems to occur. In countries and localities
where dentists are in short supply, much of the
responsibility for first-level oral health care is
assigned to a primary health care worker who
resides in the community. In some places these
individuals have been trained to provide dental
examinations and to perform nonsurgical pro-
cedures such as calculus removal, application of
topical fluorides, and the placement of sealants

and glass ionomer restorations.54 Under such a
system, much of the preventive care is provided
by people who are already part of the health
care system in the community, and the more
scarce and expensive personnel are used mainly
as a second-level referral resource.
In circumstances of extreme shortage of
trained oral health care professionals, the
concept of primary health care tries to give to
individuals as much practical information as
possible for their own care and provides guid-
ance for nondental health care workers when it
is necessary for them to place temporary fillings
or extract teeth.27
Dental care can be provided in ways that are
markedly different from those in North
America. If at first some of these alternative
ways of meeting the needs of people seem
unusual, it must be remembered that the system
that seems right for any particular country is
determined by a combination of its history, eco-
nomics, cultural traditions, and prevailing
philosophies on rights and responsibilities of
health care.
QUALITY ASSURANCE
Regardless of the way that the care system is
organized, every dental professional wants to
provide the best possible care. However, defining
what is meant by quality, and then reaching
agreement on how to attain it, continue to be a
major challenge. A typical dictionary definition
of quality is “degree of excellence.” Schoen58
defined quality in dental care as “that characteris-
tic that relates to the effective and efficient main-
tenance of optimum oral health when present,
and improvement of oral health when needed.”
Although this definition gives us the general idea
of quality in dental care, it leaves much room for
disagreement about how quality is actually
measured. Terms such as effective and efficient
maintenance and optimal oral health do not have
precise definitions. This ambiguity is behind the
variety of approaches to quality assurance.
The term quality assessment is defined by the
ADA as “the measure of the quality of care pro-
vided in a particular setting.”3 Quality assurance,
in turn, is defined as:
. . . the assessment or measurement of the quality of care
and the implementation of any necessary changes to
6 The Practice of Dentistry 73
either maintain or improve the quality of care
rendered.3
The difference in these definitions is impor-
tant: quality assessment is limited to the
appraisal of whether or not standards of quality
have been met, whereas quality assurance
includes the additional dimension of action to
take corrective steps if these are needed to
improve the situation.
The most frequently used approach to qual-
ity assessment and quality assurance builds on
the concepts of structure, process, and outcome,
the classic evaluation model described by
Donabedian.28,29 The model is based on the
idea that, although the outcome of treatment is
important and should be evaluated, a desirable
outcome is more likely if the structural arrange-
ments meet adequate standards, such as with
well-designed treatment facilities, proper equip-
ment, and appropriate and properly trained
staff. A good outcome is also more likely if the
processes used, such as diagnostic methods,
treatment planning, record keeping, and the
treatment procedures themselves, follow recog-
nized protocols. Perhaps even more important,
Donabedian argues that if a less than satisfac-
tory outcome is detected, the search for the
cause is likely to be within the process of care
and the structures that support it.
Numerous dental practice assessment proce-
dures that follow the structure-process-outcome
model have been developed.50,58,69 Box 6-1 lists
examples of some of the dimensions that can be
assessed under this approach. These many
dimensions of quality can present problems,
because when people of good faith focus on
different dimensions they can disagree as to
whether quality has been attained. Further-
more, the same level of technical quality can be
commendable in one setting and inappropriate
in another. The picture can be even more confus-
ing because much of the recent literature in this
area uses different terms to describe some or all
of the dimensions of quality assurance and qual-
ity assessment. Some examples of different
terms in the literature are listed in Box 6-2.
Although the terms in Box 6-2 are not neces-
sarily equivalent to quality assurance, they do
fit easily within the broad concept. The purpose
of quality assurance is to help provide the
best possible health care. All of the items
74 Dental Practice

BOX 6-1 Examples of Dental Practice Elements That Can Be Assessed Under the Structure, Process, and
Outcome Approach

Structure Process Outcome

Facilities Management Patient satisfaction

Setting Practice
Physical structures Personnel Oral health status
Layout Patient Oral hygiene
Amenities Tooth loss
Access Records Periodontitis
Content Caries
Equipment Completeness Function
Operatories Availability Comfort
Instruments Legibility Esthetics
Supplies
Sterilization Diagnosis Completion of treatment
Appropriateness Timeliness and appropriateness
Personnel Documentation
Types Thoroughness Recall pattern
Training Frequency
Licensure Treatment plan Needs at recall
Certification Written plan
Continuing education Sequencing
Appropriateness
Administration
Procedures Treatment
Record system Appropriateness
Protocols Timeliness

BOX 6-2 Quality-Related Terms in the Literature proliferation of terms, rather than representing
competing approaches to quality assurance,
Quality improvement60 represents the development and refinement of
Continuous improvement24 the methods to implement quality assurance.
Continuous quality improvement42
Evolution of Quality Assurance
Quality ensurance69
Quality management60 We could begin with the work of Florence
Total quality management35 Nightingale, who gathered hospital statistics in
Outcomes management70 an effort to improve clinical outcomes.51 An
Clinical practice guidelines68 important milestone in medicine was the
Practice parameters4,5 Flexner report,32 which led to a major overhaul
Standards of practice43 in the education of physicians in North America
Evidence-based clinical guidelines49 that in turn affected medical practice. The publi-
Best practices40 cation of the Gies report on dental education34
Report cards38 was a similar milestone for dentistry and dental
Risk prevention53 education. One result of the Gies report was the
eventual closure of proprietary dental schools
in the United States and the development of a
are potential tools to accomplish this goal, and system of accreditation of dental schools that,
they all fit comfortably within the structure- with refinement, continues to this day (see
process-outcome paradigm. In that sense, the Chapter 1). An example of these continuing

refinements is that, since the late 1980s, the
Accreditation Standards for Dental Education
Programs of the ADA’s Commission on Dental
Accreditation have included an explicit require-
ment for a formal system of record review.
Activities that can legitimately be included as
part of quality assurance in dentistry go back as
far as the aptitude testing and scrutiny of the
academic credentials of dental school appli-
cants. The process of accreditation of the dental
schools themselves is also part of quality assur-
ance, as are the processes to acquire and period-
ically evaluate the faculty members who teach
in these schools. The requirements for entering
dental practice are also part of the quality assur-
ance process. In most of the high-income coun-
tries there is a requirement for graduation from
a properly accredited dental school, and vir-
tually all states within the United States also
require the passing of an independently admin-
istered set of examinations.
Furthermore, requirements for periodic con-
tinuing education for renewal of licensure, the
establishment of peer bodies to review and
adjudicate complaints against clinicians, and,
when all else fails, the use of the legal system to
resolve disputes between patients and providers
of care can all be viewed as part of quality assur-
ance. The development, testing, and certi-
fication of dental materials, devices, and
equipment are also important quality-related
functions.
Recent Emphasis in Quality Assurance
Although a broad spectrum of activities legiti-
mately is part of quality assurance, most of the
attention to quality assurance in dentistry in
recent decades has focused much more nar-
rowly on dental practice itself. This recent
emphasis on formal quality assurance activities
in the United States has been attributed to the
following five influences.26
1. Rapid Growth of Dental Prepayment with
Associated Cost and Quality Concerns
Before 1970, almost all payment for dental care
in the United States was made by the individual
patient. Government and third parties had little
involvement. By about 1985, however, the pro-
portion of the U.S. population with some form
of prepayment for dental care approached 50%.
This rapid change propelled third parties
6 The Practice of Dentistry 75
into the dental care delivery system, and they
brought collective interest in the overall cost of
the insurance programs. Along with cost con-
cerns came concerns about the quality of care.
2. Rapidly Rising Health Care Costs
Because both government and private pur-
chasers were increasingly involved, there was
great concern when it became evident that the
costs of care were increasing faster than the
overall rate of inflation in the economy. It was
clear that if the costs of health care were not
brought into line with overall cost increases,
less and less money would be available for
other desired purposes.
3. Professional Standards Review Legislation
Dentistry has also been influenced by the gen-
eral climate of increasing demands for account-
ability that have been imposed on medical and
hospital care through legislation. Especially
since the advent of Medicare and Medicaid in
1965, government funds account for a large and
growing part of medical care expenditures,
and as a result requirements related to quality
assurance have been imposed on medical and
hospital-based care. Even though government
involvement in the payment for dental care in
the United States is small, dentistry has been
affected both directly and indirectly by this
increasing climate of accountability.
4. Growth of Consumer Involvement
Over the past several decades there has been an
increase in the interest of consumers, as a group,
in issues related to all sorts of services and prod-
ucts. Dentistry has been affected by this general
movement, especially in the sense that it has cre-
ated a climate in which providers of services are
seen as being far more subject to scrutiny than
had previously been the case.
5. Malpractice Litigation
Perhaps also related to the growth in con-
sumerism, individual patients have become far
more likely to seek relief through the legal sys-
tem to redress perceived shortcomings in the
care that they receive. One result has been the
growth of quality-related activities such as risk
prevention and development of standards of
care, in an effort to reduce the likelihood that
such lawsuits will need to be undertaken.
76 Dental Practice
Examples of Quality Assurance
Activities:The Dimensions of Quality
The types of activities that are part of quality
assurance in dentistry illustrate the wide scope
of the field. The following seven topics are rep-
resentative of quality assurance approaches in
dentistry.
1. On-Site Evaluation of Dental Practice
On-site evaluation of dental practice is perhaps
the most widely used form of quality assurance,
especially for programs directed by third-party
payers. Various combinations of structure,
process, and outcome are measured by trained
auditors who visit the dental office. Although
there are numerous examples of this approach
in the dental literature,50,58,69 it is the subject of
many concerns. For one thing, the process is
expensive. It is time consuming for a trained
evaluator to visit each dental office and to
conduct what is usually a highly detailed assess-
ment. Marcus,47 who has considerable experi-
ence with this approach to quality assurance,
has stated the following:
I am not convinced that our quality assurance efforts
have had a significant impact on improving the process
of care, nor has it been effective in eliminating those
providers who are unwilling to change their pattern of
care delivery.47
The work of van der Wal and colleagues69
also casts uncertainty on the validity of the
process. This group was unable to find the
expected associations between structural aspects
and outcomes of dental care. Although there is
much room to debate the validity and complete-
ness of both the structure and outcome meas-
ures used in their study, it nevertheless does raise
several important points. First, this study adds to
the concern that the structure-process-outcome
paradigm has not been empirically shown to
represent accurately the “real world.” It contin-
ues to be unsettling that we cannot produce
good empirical evidence of the connection that
is so widely believed to be present. Second, the
authors suggest the possibility that the structural
characteristics included in dental office evalua-
tions are now so well known to dentists that vir-
tually all are in compliance, so that structural
indicators are no longer valid predictors of
outcomes.
2. Audit of Dental Records
In addition to the assessment of technical qual-
ity of restorations, the record audit as a quality
assurance mechanism is perhaps the most
highly developed and widely used approach for
institutions20 such as dental schools and hospi-
tal dental departments.6 In hospitals, record
audits fit well with the approach that has been
used for a long time in medicine for hospital
accreditation. In dental schools, it fits well with
the traditional teaching functions. Through the
detailed review of dental records, not only can
the dental care provided by the institution be
assessed, but the student is also exposed to a
review of the rationale and process of patient
management and care.
As with several of the other approaches to
quality assurance, the audit of dental records is
a relatively expensive and time-consuming
process. Apart from the institutional settings in
which they are required by external auditors,
record audits are not widely used.
3. Technical Quality
Assessment of the technical quality of restora-
tive procedures has perhaps the most highly
detailed criteria but is also one of the least-used
forms of quality assurance in dentistry. First of
all, measurement of technical quality is expen-
sive. It is time consuming for examiners, and it
is difficult to get cooperation from more than a
small fraction of the patients who are selected
for evaluation. Further, the results from random
audits have not been encouraging, partly
because of the low turnout of patients and also
because unacceptable care is so infrequently
found.25 Because of the high costs and low
yield, direct assessment of technical quality has
not developed into a major area of quality
assurance.
4. Oral Health Status
If there were a simple, valid, sensitive, and easily
measured index of oral health status, the job of
quality assurance would be much easier. After
all, the ultimate objective of oral health care is
to help patients attain and maintain the highest
possible level of oral health.
Although there have been noteworthy efforts
to develop such indexes of oral health,48,52 their
acceptance has been limited, and there has
been little progress in this direction in the

past decade. These indexes are discussed in
Chapter 14.
5. Appropriateness of Care
Appropriateness of care is a dimension that has
so far received little attention in dentistry. There
is general agreement that the use of a technically
superior restorative procedure when it is not
needed is not acceptable quality. Standards for
the appropriate use of dental care nevertheless
continue to elude clear definition.
6. Consumer Satisfaction
Work in the area of consumer satisfaction is also
in its infancy, but it is currently of considerable
interest, especially to purchasers of group den-
tal insurance. One of the primary reasons for
employers to purchase dental insurance for
their employees and their families is to make
the employee happy and loyal to the employer.
Although these purchasers are certainly inter-
ested in the oral health of their employees, of
considerable importance is the satisfaction of
these employees with the dental benefit. As a
result, purchasers are increasingly pressing for
measures of consumer satisfaction.
7. Profiling of Dental Providers
With the advent of computer-based records of
dental treatment, especially in insurance com-
panies, there have been attempts to make use of
these kinds of data to evaluate the quality
of dental care indirectly. If successful, this
approach could be much less expensive than
the direct methods already discussed. The
idea is that by aggregating treatment records
from large numbers of providers across many
patients, inappropriate patterns of care can be
detected and corrective actions taken.39,62 At
least in theory, this approach offers consider-
able promise. Not only can potentially inappro-
priate use of care be identified cross-sectionally,
but patterns of care in individual patients over
time also can be used to permit inferences
about the effectiveness and appropriateness of
the care provided.
Quality Assurance and Cost Control
In the often-heard accusations that quality
assurance is being misused as a tool for cost
control is the implication that quality and
cost control are incompatible. However, an
6 The Practice of Dentistry 77
honest view of quality assurance must accept
that quality assurance may result in higher
costs. There is no doubt that quality assurance
activities themselves are costly and that quite
often they identify deficiencies that cost money
to rectify. Quality assurance and cost control are
not only compatible; they must be considered
together for truly meaningful quality assurance.
Important to the issue of quality assurance is
the fact that there is not, nor will there ever be,
an unambiguous, universal, and stable formula
for what constitutes quality dental care. The def-
inition at any one time and place must be con-
ditional on what is possible (the state of the
science and art of dentistry) and what is afford-
able to the individual and to society. Even in
the richest of societies, resources are finite.
Therefore it follows that the definition of what
constitutes quality dental care is a continuously
variable one, and it will inevitably include con-
sideration of cost.
Because cost considerations are fundamen-
tally part of quality, it follows that if there are
two or more equally effective and acceptable
ways of reaching a desired outcome, the least
expensive one (i.e., the most efficient one) is of
higher quality. Simply put, if the desired out-
come can be reached with fewer resources, the
excess resources can be used by the individual
and society to pursue additional desired goals,
and the individual and society will be better off.
This philosophy illustrates the fundamental
role of cost in the quality equation.
Nevertheless, the tensions between quality
assurance and cost containment are consid-
erable. On the one hand, if cost containment
reduces unnecessary care, quality should increase.
On the other hand, substitution of lower-cost
services might reduce the quality of care. Bailit19
has pointed out that cost containment is not
likely to be as simple as reducing so-called
unnecessary services; the more expensive treat-
ments usually do produce benefits for individ-
ual patients. Nevertheless, the same amount of
money could often produce even more benefit
for a large number of people if it were used for
other, less expensive services.
Although it has been said that better-quality
care is more expensive, the converse is not
necessarily true: more expensive care is not nec-
essarily of better quality. If too much of
the available funds goes to a small number of
78 Dental Practice
the patient group, the overall oral health of the
group may well suffer. This emphasizes a
dilemma that is discussed further in Chapter 7,
which is that there is no inherently “right”
amount of health care. The amount of money
that any individual, group, or society as a whole
will want to spend for a particular health care
procedure, or for health care in general, can be
determined only by balancing it against other
needs and desires. Implicit in this idea is that
there is such a thing as too much health care,
even if the use of a service can be shown to
improve the medical or dental condition of a
person. If the resources required to provide such
a service are so large that other even more bene-
ficial services cannot be provided, then it would
be rational for individuals and society to con-
clude that such a procedure should not be used.
It has become more obvious with third-party
payments that when there is a finite amount of
money for care, priority decisions must be made
as to who receives services, what services may be
provided, or both. How these priorities will
be set and how the inevitable trade-off between
the benefit to the group versus the individual
patient will be resolved will continue to be a
topic of debate.
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dental franchise industry. J Dent Pract Admin 1988;
5(1):21-4.
 7 Financing Dental Care
INSURANCE PRINCIPLES AND DENTAL CARE
EXPENDITURES FOR HEALTH CARE
EXPENDITURES FOR DENTAL CARE
FEE-FOR-SERVICE DENTAL CARE
THIRD-PARTY PAYMENT IN DENTISTRY
Growth of Third-Party Payment in Dentistry
Reimbursement of Dentists in Third-Party
Plans
NOT-FOR-PROFIT DENTAL PLANS
Delta Dental Plans
Reimbursement of Dentists in Delta Plans
Blue Cross and Blue Shield Plans
FOR-PROFIT DENTAL PLANS
Commercial Insurance Plans
MANAGED CARE
Dentistry in Managed Care
Health Maintenance Organizations
Preferred Provider Organizations
Health care historically has been provided on
a fee-for-service basis, in which the patient
pays the provider directly for services. This two-
party system is a private contract involving only
the provider and the patient. Methods of financ-
ing health care in the United States, however,
have progressed far beyond this traditional sys-
tem since the mid-1930s and especially since
1965. A fundamental change has been the emer-
gence of third parties, meaning that the financ-
ing of health services is no longer a matter of a
purely private contract between provider and
patient. In 2001, for example, 86% of the total
outlays for health services and supplies involved
a third party, and 46% of all health care
services were paid for by government funds.57
Dentistry’s entry into the third-party system has
been more recent, but third-party involvement
in the payment for dental care is now a major
and still-evolving part of dental practice.
This chapter reviews the various mecha-
nisms used to finance dental care and the
Point-of-Service Plans
Concerns Regarding Managed Care
DIRECT REIMBURSEMENT
DISCOUNT DENTAL PLANS
ADMINISTRATIVE SERVICES ONLY
MEDICAL SAVINGS ACCOUNTS, HEALTH
SAVINGS ACCOUNTS, AND FLEXIBLE
SAVINGS ACCOUNTS
FORCES AFFECTING THE DESIGN OF
THIRD-PARTY DENTAL CARE PROGRAMS
PUBLIC FINANCING OF HEALTH CARE
Public Expenditures for Dental Care
Medicare
Medicaid
State Children’s Health Insurance Program
Other Programs of Public Financing for Dental
Care
National Health Insurance
effects that these mechanisms have on care
provision.
INSURANCE PRINCIPLES
AND DENTAL CARE
To understand how dentistry fits into third-
party payment, a review of insurance principles
is helpful. During the years after World War II,
when medical insurance was growing rapidly,
dental care was one of the “fearful four” areas
of health care (dental care, psychiatric care,
prescription drugs, and long-term care) con-
sidered uninsurable by commercial insurers.
This reasoning was based on the assumption
that the nature of dental need violated the
basic principles of insurance,22 which state
that to be insurable a risk must be the following:
●
Precisely definable.
●
Of sufficient magnitude that, if it occurs, it
constitutes a major loss.
●
Infrequent.
81
82 Dental Practice
●
Of an unwanted nature, such as destruction
of a home through fire.
●
Beyond the control of the individual.
●
Without “moral hazard,” which means that
the presence of insurance itself should not
lead to additional claims.
All health insurance violates some of these
principles. For example, many of the benefits
paid by health insurance represent relatively
small amounts of money, and people with
insurance are more likely to use care than those
without it.37,42 Insurance carriers found they
could get around these problems in several
ways, such as the following:
●
Having patients pay a share of the costs.
●
Limiting the range of services covered.
●
Offering coverage only to groups.
●
Including waiting periods after enrollment
before benefits became payable.
●
Using preauthorization and annual expen-
diture limits.
Requiring patients to pay part of the cost of
some services is an economic disincentive to
overutilization. The portion of the cost of the
service that a patient pays is either a deductible
or coinsurance (sometimes called copayment).
A deductible is a set amount of money that the
patient must pay toward the cost of treatment
before benefits of the program go into effect.4
A familiar example of a deductible is the “front-
end” payment of a claim under automobile
insurance. Coinsurance means that the patient
pays a percentage of the total cost of treatment.4
For example, if a patient is to pay 20% of the
cost of an amalgam restoration, the amount
the patient must pay varies depending on the
approved fee for an amalgam but in any case
will be 20% of that fee.
Insurance carriers also limit the range of
health care services covered: some services are
paid for and some are not, according to the
plan. This is termed coverage, covered charges, or
schedule of benefits. Examples of services that are
not usually covered in dental policies are
implants (although this is changing as implants
become more common), cosmetic procedures,
and extensive treatment for temporomandibu-
lar joint disorder. A common point of confu-
sion is that, when a service is not covered by
insurance, some patients take it to mean that
they cannot have it, that the insurance company
is somehow denying this service to the patient.
This is not the case; it is simply that the patient,
rather than the insurer, is responsible for the
payment.
An additional cost-control mechanism, preau-
thorization (sometimes called predetermination),
means that treatment plans for more than a speci-
fied amount, or for especially costly services,
must be reviewed by the carrier’s dental consult-
ants to ensure that the proposed treatment is rea-
sonable and that the same quality of care could
not be achieved at less expense.
Health insurance was at first offered only to
groups, because illness experience is reasonably
predictable for a group but much less so for an
individual. The risk of adverse selection, which
means the inclusion of too many high-risk ben-
eficiaries, was reduced because insuring only
large groups averaged out the risks. Although a
large group would likely include people with
high levels of need, there would also be many
who had little need for care and who would still
pay premiums. In fact, this is the essence of
insurance. The fact that the cost of care required
for a few people far exceeds the premiums paid
for them is irrelevant as long as the average cost
of care across the group is in balance with the
premium.
The probability of adverse selection was fur-
ther reduced by the use of waiting periods after
enrollment. The waiting period ensured that
people with existing disease were not simply
going to use the plan to have that condition
treated and then drop out. As experience
with the administration of health insurance
grew, carriers were able to offer individual poli-
cies. Today, many commercial and nonprofit
insurance carriers make individual policies
available for hospital and major medical cover-
age, although premiums are considerably
higher and benefits are often more limited than
for group policies.
After looking at the list of insurance princi-
ples, one can see why dental care was for a long
time considered uninsurable. Nearly everyone
has some dental treatment needs. They tend to
be frequent rather than infrequent, and unlike
the cost of hospital care the cost of dental treat-
ment is rarely catastrophic. Nevertheless, evalu-
ations of some of the earliest group prepayment
plans indicated that dental care indeed was
insurable because cost was found to be not the
only barrier to dental care;49–51 even when the

cost barrier was removed, potential patients did
not pour in as many had expected. Although
utilization of dental service was increased, it
stayed well short of 100%. In other words,
although all members of the group may have
needed dental care and all were paying a pre-
mium toward it, only some members were seek-
ing treatment. Indeed, if 100% of the group
seeks dental care on a regular basis, it might be
less expensive for them to pay for their care
individually rather than through prepayment.
EXPENDITURES FOR HEALTH CARE
Expenditures for health care have risen sharply
in all industrialized countries over the last sev-
eral decades, but nowhere has this pattern been
as pronounced as in the United States. Fig. 7-1
shows that, in 1929, expenditures in the United
States for health care (including dental care)
accounted for 3.6% of the gross domestic prod-
uct (GDP). Since 1929, the amount has gone
steadily upward, reaching 14.9% of GDP in
2002.26,57 Predictions suggest that spending for
health care could rise to 20% of the GDP in the
next few decades,23,66 a level of national expen-
diture that is a cause for deep concern.
Fig. 7-2 shows how the per capita national
health expenditures have risen since 1960.
From an annual average of $141 in 1960, the
average cost per person had risen to $5440 in
16
14
12
10
Percent
0
1929 1940 1950
Fig. 7-1 National health expenditures as a percentage of the gross domestic product in the United States, selected
years, 1929-2002.26,36,57
7 Financing Dental Care 83
2002, a truly daunting figure.36,57 For insurance
to be able to cover these kinds of costs, it is easy
to see why premiums must be high. Fig. 7-2 also
shows that the portion of the cost of health care
paid by public funds has grown since 1960. In
2002, 46% of total national health expenditures
were paid by public (government) funds.57
Some of the reasons given for this increase in
the cost of health care in the United States
include the following six factors:
Increasing Costs Incomes of health care
workers have risen faster than the incomes for
many other workers.
Difficult Economies of Scale It is harder to
achieve economies of scale in health care than
in many other sectors of the economy. In many
manufacturing industries, for example, it does
not require 10% more workers to produce an
additional 10% of a product. In health care, by
contrast, increasing the amount of care pro-
vided requires a nearly proportional increase in
the workforce.
The Practice of “Defensive” Medicine Tests
carried out to protect the provider against possi-
ble litigation, rather than to treat the patient,
lead to a rise in costs.
The Aging Population An aging population
causes an increase in per capita costs. Because
older people use more health care services,
the average cost of care will increase as the average
age of the population increases. In addition, the
1960 1970 1980 1990 1995 2002
Year
84 Dental Practice
6000
5000
4000
Dollars
3000
2000
1000
0 cannot continue to climb indefinitely, because
1960 1970 1980 1990 1995 2002
Year
Public
Private
Fig. 7-2 Per capita national health expenditures, showing
the proportionate expenditure of private and public funds in
the United States, selected years, 1960-2002.36,57
expectation of longer life brings a greater will-
ingness to provide heroic care for a person
who in earlier days would not have been
expected to live much longer even if healthy,
but who today is thought to have a reason-
able chance for more high-quality years of
life.
Developments in Technology Some innova-
tions reduce the costs of care because they are so
much more effective than any available alterna-
tives (antibiotics, for example, reduced the aver-
age length of a hospital stay when they were
introduced in the 1940s and 1950s). Others,
because they are providing care that was previ-
ously unavailable, can only add to aggregate
costs. An example is treatment for end-stage
renal disease for patients who in earlier days
would have soon died. With dialysis they now
live, but at a cost that was estimated to average
$24,976 per patient per year as long ago as
1983.48
Third-Party Payment Insurance has provided
large amounts of money for care that would
otherwise have been unavailable. For example,
many of the elderly and the poor who receive
the benefits of Medicare and Medicaid would
not otherwise have had the money to pur-
chase this care. Without these programs, the
total and per capita costs of care would
undoubtedly be smaller. The same is true for
private insurance, because many who otherwise
would have faced large bills for hospitalization
and other services would have been forced to do
without.
The spiraling costs of health care present
American society with a classic trade-off
dilemma. On the one hand, if people go with-
out health care that can improve or prolong
their lives, both the individual and society suf-
fer. On the other hand, it should be evident that
the proportion of the GDP going to health care
as more of our available resources go to health
care there is less for housing, education, recre-
ation, and other necessities that contribute to
health, wealth, and happiness. Although there
is ample reason to be concerned for people who
receive too little health care, there is also the
possibility that a point can be reached at which,
at least in the aggregate, there is too much
health care relative to life’s other necessities.
The dilemma is made even more difficult by the
fact that, as of 2002, 43.6 million people in the
United States had no health insurance.56
Although there is a justifiable outcry that some
form of coverage should be provided for these
people, it is also obvious that to do so will fur-
ther increase national expenditures.30,42,78
Health care providers, in their honest desire to
do the best for their patients, need to recognize
that this tension between the individual and
society will always exist.
Resolution of this dilemma is made even
more complex by the inclusion of government
and private third-party agencies in the equation.
Because the total costs of care continue to climb
and put more and more pressure on the eco-
nomy, and because most health care costs are
paid through third parties, the pressure for col-
lective action to control these costs will con-
tinue. No one in health care should be surprised
to see a continuing stream of proposals aimed
at controlling or reforming the health care
system.
EXPENDITURES FOR DENTAL CARE
Expenditures for dental care, although only a
fraction of the total for health care, are neverthe-
less substantial. Fig. 7-3 illustrates that the total
expenditures for dental care by Americans grew
from less than $500 million in 1929 to an esti-
mated $70.3 billion in 2002.16,36,57 This latter
 7 Financing Dental Care 85

80

70

60
Billions of dollars

50

40
Fig. 7-3 Total expenditures for
30 dental care in the United States,
selected years, 1929–2002.36,57
20

10

0
1929 1940 1950 1960 1970 1980 1990 1995 2002

Year

16

14

12

10
Percent

8
Fig. 7-4 Per capita expenditure
for dental care as a percentage of
6 total health expenditures in the
United States, selected years,
4 1929–2002.26,36,57

0
1929 1940 1950 1960 1970 1980 1990 1995 2002

Year

figure represents an average per capita expendi-
ture for dental care of $250 in 2002.
Figs. 7-4 and 7-5 present two additional views
of the cost of dental care. Fig. 7-4 shows that, rel-
ative to the total cost of personal health care
expenditures, dental expenditures have fallen
steadily from the 14% reported in 1929 to 4.5%
in 2002.26,57 This pattern reflects the combina-
tion of the steep rise in the overall costs of med-
ical care and the more modest rise in the costs of
dental care. Fig. 7-5 presents the expenditures
for dental care as a percentage of the GDP. The
pattern here is especially interesting: the relative
decline from 1929 to 1950 corresponds to the
period of the Great Depression followed by
World War II. Dental care is income and price
elastic, so that, as real income fell during the
depression and as the cost of other goods and
services rose during and after the war, there was
simply less money available for dental care. The
rise since 1970 coincides with a period of growth
in real income and also in the extent of dental
insurance. Economic theory suggests that both
of these changes should result in a relative
growth in dental expenditures, a phenomenon
that has indeed occurred. The relative growth in
dental expenditures has continued up to the
present, to about 0.67% of the GDP in 2002,
even though the percentage of the population
covered by dental insurance has plateaued.57
This is a sign that the dental sector continues to
be a robust part of the national economy.
86 Dental Practice
Percent 5
0
1929 1940 1950
Fig. 7-5 National health expenditures for dental care as a percentage of the gross domestic product in the United
States, selected years, 1929-2002.26,36,57
FEE-FOR-SERVICE DENTAL CARE
Private fee-for-service payment, the two-party
arrangement, is the traditional form of reim-
bursement for dental services in the United
States and elsewhere. Under this system, the
patient decides when to visit a dentist, and the
dentist suggests appropriate treatment and
informs the patient of the fee for the service. If
the patient chooses to follow the recommenda-
tions of the dentist and receives the services, the
patient is then responsible for the fee. As shown
in Fig. 7-6, as recently as 1970 almost all pay-
ments for dental services came directly from
patients.36 However, by 2002, because of the sub-
stantial growth in prepayment, direct consumer
payment had dropped to about 44% of all pay-
ments, with nearly 50% being paid by private
insurance.57
THIRD-PARTY PAYMENT
IN DENTISTRY
In the language of contracts, the patient and
dentist are the first and second parties, and the
administrator of the finances is the third party,
defined as the party to a dental prepayment
contract that may collect premiums, assume
financial risk, pay claims, and provide adminis-
trative services. Third-party payment for dental
services therefore is payment for dental care that
involves another party rather than payment
directly by the patient. The third party is some-
1960 1970 1980 1990 1995 2002
Year
times called the carrier, insurer, underwriter, or
administrative agent. The purchaser of the plan
can be an organized private group such as a
union, or it can be an employer, a union-
employer welfare fund, a governmental agency,
or an individual. Usually, however, the term
third party, without further qualification, refers
to an insurance company. When the govern-
ment acts as the third party, the term more com-
monly used is public financing of care.
Growth of Third-Party Payment in Dentistry
In private third-party plans, periodic premiums
are collected to meet the costs of providing care
as well as the administrative costs of the third
party. It has been argued that this arrangement
should most properly be called prepayment
rather than insurance, because it does not fulfill
the classic definitions of insurance. Be that as it
may, the term dental insurance has entered the
language, and the terms dental prepayment and
dental insurance as commonly used are virtually
synonymous. The main difference between den-
tal and some other forms of insurance is that
traditional insurance involves a group of people
making relatively small payments to cover the
risk of a few suffering catastrophic loss, such as
the loss of a home through fire. The expectation
is that few of them will ever collect any insur-
ance payments. Dental prepayment, on the
other hand, is a mechanism to spread the finan-
cial load of dental care over a group and over
time. Virtually all members of the group can

100
80
60
Percent
40
20
0
1960 1970
Fig. 7-6 Proportion of total dental care expenditures paid by consumers out of pocket, by private insurance, and by
government funds in the United States, selected years, 1960-2002.36,57
reasonably expect to make regular and some-
what predictable use of the benefits.
For companies that administer these plans,
the method for setting the premiums is essen-
tially the same as it is for any other form of
insurance. Based on the type of benefits
involved and the characteristics and previous
history of a group, the actuaries estimate how
much dental care will be provided to the group
in the coming period of time (usually at least 1
year). The expected reimbursable cost of that
care plus the administrative expenses form the
basis for premium calculations. Most private
dental insurance in the United States is avail-
able only through group purchase; there are few
individual policies. Individual policies that are
available are characterized by high premiums or
limited benefits. This is the carriers’ method of
countering the risk of high use and adverse
selection.
Who actually pays for third-party care? A
union that negotiates a dental plan as a fringe
benefit is choosing to accept the plan rather
than cash wages, so the union members pay for
it in wages foregone. Ultimately, if the compa-
nies employing the union members increase
the price of their products to finance the plan,
the purchasers of those products pay for it.
Reference to the third-party agency as the “payer
for services,” although common, is incorrect;
nor are the union members getting “free” care,
even if they do not pay directly out of pocket.
Passage of the Taft-Hartley Act in 1947
allowed labor unions to seek fringe benefits, in
7 Financing Dental Care 87
Out of Pocket
Insurance
Government
1980 1990 1995 2002
Year
addition to wages, through collective bargain-
ing. Since then, health care insurance has been a
popular fringe benefit. One of the reasons for
this popularity is that the premiums paid by the
employer are not usually counted as taxable
income for the employee. Each dollar of earn-
ings taken in the form of health insurance there-
fore buys more health care than if it is taken
as cash wages, because cash wages are taxed
whereas the insurance benefits are not. (Health
insurance as a fringe benefit, with protection
from tax, is popular with the insurance and
health care industries, too, because it actually is
a subsidy for them.) There have been frequent
unsuccessful attempts at the federal level to
limit the amount of these health insurance
premiums that are protected from taxes. It is
reasonable to expect periodic attempts of this
type in the future in times of budgetary diffi-
culty. Such a “tax cap,” if it were enacted, would
reduce the popularity of dental insurance. It is
assumed that if such a limit were to be placed
on the tax deductibility of health insurance
premiums, most people would apply the tax-
deductible amount to their hospitalization and
medical insurance. This would mean that the
money paid by employers for dental insurance
would be treated as taxable income, and addi-
tional wages would be deducted from each pay-
check to pay this tax. Dental insurers fear that
this change would cause some individuals and
groups to drop their dental insurance.
By the late 1960s, with some 85% of the
American population covered by hospital and
88 Dental Practice
surgical expense insurance,33 coverage for den-
tal expenses emerged as a popular area for nego-
tiation by labor groups seeking additional
fringe benefits. Growth of dental prepayment
plans through the 1970s and 1980s therefore
can be seen as an evolutionary step in the
growth of employment fringe benefits.
The rapid growth of prepayment since 1970
has changed the nature of dental practice. The
growth is illustrated in Fig. 7-6, which shows
that the portion of dental care costs paid by pre-
payment plans increased more than tenfold
between 1970 and 2002. The proportion of the
U.S. population covered by some sort of dental
insurance increased from less than 5% in 1970
to well over one half by the turn of the century.
Today it is a rare dental practice indeed that sees
no insured patients at all. In many parts of the
country, the majority of the patients in most
practices have dental insurance.
Although the growth in dental insurance has
been spectacular since 1970, further rapid
growth in the immediate future is not likely. This
is because members of the large unions in the
major U.S. industries are, for the most part,
already covered. For dental insurance to grow,
mechanisms will have to be developed to reach
small businesses and individuals. A second rea-
son why dental insurance will grow only slowly
is the general climate of cost control in all aspects
of business, which in turn comes from the fierce
demands on the United States to be competitive
in the global economy. Increased concern for
worldwide competitiveness works against offer-
ing benefits to workers not already covered, and
there are already some signs of cutbacks in some
industries. A third factor that may work against
further expansion of dental insurance is the
improvement in oral health, which is especially
evident in young adults and children (see
Chapters 19-21). It may be that because people
in these younger age cohorts have experienced
little need for expensive and unexpected dental
treatment, they will not push their employers as
hard for dental insurance as did their elders, who
had much higher levels of need for treatment.
Reimbursement of Dentists in Third-
Party Plans
Control of the costs of third-party plans is
essential to their success, for if the insurance
plan is seen as a bottomless money pit, the plan
will have to raise premiums to higher and
higher levels, which makes it unlikely that any-
one will be willing to buy the policy. Because
the implications of “control” in this context are
anathema to most practitioners, methods of
reimbursing dentists under third-party plans
have long preoccupied the American Dental
Association (ADA). The ADA sees the need for
controls but also tries to maximize the inde-
pendence of the dental practitioner. Major
forms of third-party reimbursement currently in
use are:
●
Usual, customary, and reasonable (UCR)
fee
●
Table of allowances
●
Fee schedule
●
Discounted fee (preferred provider organi-
zations [PPOs])
●
Capitation
In line with its philosophy of maximizing
practitioner independence, the ADA has consis-
tently supported the concept of the UCR fee as a
reimbursement method for dentists in prepay-
ment plans. However, ADA resolutions that
UCR fees should be the preferred method
of reimbursement were rescinded on legal
grounds after the U.S. Supreme Court decision
in June 1975 in Goldfarb v. Virginia State Bar
et al. This decision ruled that learned profes-
sions were not exempt from antitrust laws.5,7,8
In effect, the Court said that each practitioner
should be free to choose how he or she wants to
be reimbursed and that it was inappropriate for
a professional association to suggest to its mem-
bers which choice to make.
Usual, Customary, Reasonable Fee
The ADA definitions of usual, customary,
and reasonable fees are as follows:
Usual fee: The fee that an individual dentist
most frequently charges for a given dental
service
Customary fee: The fee level determined by
the administrator of a dental benefit plan
from actual submitted fees for a specific
dental procedure to establish the maxi-
mum benefit payable under a given plan
for that specific procedure
Reasonable fee: The fee charged by a dentist for
a specific dental procedure that has been
modified by the nature and severity of the
condition being treated and by any med-

ical or dental complications or unusual cir-
cumstances, and that therefore may differ
from the dentist’s “usual” fee or the benefit
administrator’s “customary” fee4
When third-party dental programs first
began, many dentists were opposed to them on
the grounds that they would be forced to adopt
lower fees than those that they usually charged.
The evolution of the UCR fee concept as a
mechanism acceptable both to dentists and car-
riers has allowed third-party dental care to be
provided while still permitting individual
dentists to charge what they believe their serv-
ices are worth. It is reasonable to suggest that
dental prepayment plans would not have been
accepted by dentists to the extent they have
been without the UCR fee concept.
Table of Allowances
A table of allowances (or schedule) is defined
as a list of covered services with an assigned dollar
amount that represents the total obligation of the
plan with respect to payment for such service but
that does not necessarily represent the dentist’s
full fee for that service.4 For example, if a dentist’s
usual fee for a particular service is $20 and the
plan lists a fee of $15 as payable for that service,
the dentist will provide the service, collect $15
from the carrier, and may charge the patient $5 to
make up the difference. Under the UCR fee
method, on the other hand, the plan pays the
dentist’s usual fee in full (less any required patient
copayment), in this case $20. Use of a table of
allowances as a method of reimbursement
requires that dentists carefully explain to patients
the limited nature of the insurance payment,
because some patients are unaware that their plan
may not cover the costs in full.
Fee Schedule
A fee schedule is defined as a list of the
charges established or agreed to by a dentist for
specific dental services.4 A fee schedule is usu-
ally taken to represent payment in full, whereas
a table of allowances, as just explained, may
not. With a fee schedule, the dentist must accept
the listed amount as payment in full and not
charge the patient at all. Fee schedules for den-
tal care are sometimes established by public
programs, such as Medicaid in many states.
Dentistry’s opposition to fee schedules is based
on (1) the potential inflexibility of such sched-
7 Financing Dental Care 89
ules, meaning that the fees listed can fall below
customary fees, particularly in times of rapid
inflation; (2) the implicit assumption that all
dentists’ treatment is of the same quality and
therefore worth the same fee; and (3) the fear
that autonomy is threatened, especially if the
fee schedule is not controlled by the dentists.
A potential risk with use of a fee schedule is
that, if the fees paid are too far below the usual
level, few dentists will be willing to treat the
covered patients. This has been cited as one rea-
son why many dentists either severely limit the
number of their Medicaid patients or refuse to
accept such patients altogether.17,35,64
Discounted fee
Discounted fees are usually the basis for PPO
plans. Participating dentists have agreed to pro-
vide care for fees that are usually lower than
those charged by many dentists in their area.
Most preferred provider dental plans do provide
partial payment for care received from a nonpar-
ticipating dentist, but in this case the patient is
responsible for all of the difference between the
dentist’s fee and the amount paid by the plan.
Capitation
Reimbursement of the dentist by capitation,
as in a medical health maintenance organiza-
tion (HMO), became more common during the
1980s and 1990s but plays a much smaller role
in dentistry than it has in medicine. The ADA
defines capitation as a dental benefit program
in which a dentist or dentists contract with the
program’s sponsor or administrator to provide
all or most of the dental services covered under
the program to subscribers in return for a pay-
ment on a per capita basis.4 A capitation fee is
usually a fixed monthly payment paid by a car-
rier to a dentist based on the number of patients
assigned to the dentist for treatment. Capitation
requires that patients be assigned to specific
dentists or dental practices for care, so that the
capitation payment can be paid to the appropri-
ate dentist or practice. This assignment is
important, because the dentist receives a fixed
sum of money per enrolled person per month,
regardless of whether the participants in the
plan receive care during that particular month.
The assumption is that, although some patients
will need a lot of care, others will need little or
none, and therefore the total amount of money
90 Dental Practice
paid to the dentist will be sufficient to cover the
overall costs of care for the covered group.
Many dentists are resistant to capitation
because of a fear that high utilization and
demands for expensive forms of care could rap-
idly outrun the capitation fee and that dentists
will thus be at an economic disadvantage. As a
dissenting voice, Schoen45–47 argued that capi-
tation works every bit as well as fee for service
and that with proper planning it is a highly effi-
cient method of financing group dental care,
especially for less affluent groups. Despite
Schoen’s claims of success with capitation in his
own group practice, however, many dentists and
the ADA remain cautious. The ADA is opposed
to capitation and fee schedules as the sole forms
of reimbursement in prepayment plans, arguing
that where such mechanisms exist they should
be on an equal footing with UCR fees so that
prospective patients have a choice. In fact,
by the 1990s there were very few “pure” capita-
tion plans. Most capitation plans now include
copayments, especially for more expensive serv-
ices, and annual maximums, both of which
limit the economic risks faced by the dentist.
NOT-FOR-PROFIT DENTAL PLANS
Delta Dental Plans
In June 1954, the Seattle District Dental Society
in Washington State was approached by the
International Longshoremen’s and Warehouse-
men’s Union-Pacific Maritime Association with
a request that the society submit a proposal for
a comprehensive dental care program for the
children of the union’s members up to 14 years
of age. The proposal requested by the union
required information on administration, fees,
methods of operation, dental care provided,
and control of quality. At that time there was
almost no previous experience with plans of
this type. The dental society nevertheless wished
to discourage the union from setting up its own
clinics, and it developed a plan whereby the
children could be treated in the offices of pri-
vate dentists. Shortly thereafter, the first dental
service corporation was born.72 Within a few
years dental service corporations were also
formed in Oregon and California, and in subse-
quent years the idea of the dental service corpo-
ration spread throughout the country from the
West Coast.
A dental service corporation is a legally con-
stituted not-for-profit organization, incorpo-
rated on a state-by-state basis, that negotiates
and administers contracts for dental care. The
original dental service corporations, now know
as Delta Dental Plans in most states, were spon-
sored by the constituent dental societies in each
state where they were initially formed. A service
plan is a program in which the payment is
meant to represent full payment, with no addi-
tional charge to the patient allowed beyond
a preestablished copayment or deductible.
Following the success of the early Delta plans,
Blue Cross and Blue Shield organizations also
began organizing dental plans in many states,
which usually also were organized as not-for-
profit service corporations.
As the number of state dental association–
sponsored service corporations increased through
the early 1960s and the size of the groups for
which dental care benefits were negotiated
grew, the need for a national organization of
dental service organizations became apparent.
Accordingly, the National Association of Dental
Service Plans was formed in 1966, with staff
and financial help from the ADA. The name
became Delta Dental Plans Association (DDPA)
in 1969,28 and most of the member corpora-
tions became known as the Delta Dental Plan
for the particular state.
DDPA has also become the vehicle through
which the Delta plans in individual states
compete with national for-profit insurance com-
panies for contracts with companies with employ-
ees in more than one state. Through DDPA, an
organization called DeltaUSA was formed to coor-
dinate and administer these multistate contracts.
In 2003 more than 108,000 participating dentists
were available to DeltaUSA through the individ-
ual state Delta plans, accounting for at least 70%
of all dentists in practice nationwide. Collectively,
Delta plans cover approximately 42 million peo-
ple in the United States.18
The underlying philosophy of the Delta
Dental Plans was to permit dental practitioners
to adapt their traditional patterns of practice to
meet the demand for group purchase of dental
care. In this sense, Delta plans have followed the
lead of the professionally sponsored Blue Cross
and Blue Shield hospital and medical plans.
Most Delta plans were formed for the sole pur-
pose of providing dental prepayment, and most

have retained dental insurance as their sole or
major business.
Delta also pioneered specific approaches to
ensure the quality of care provided and to keep
a program’s costs under control, although other
carriers now use many of these approaches as
well. Quality of care is sometimes monitored by
posttreatment examinations, in which a sample
of individual patients who have received care
through a plan are examined by a panel of inde-
pendent consultant dentists to ensure (1) that
the care claimed and paid for was in fact pro-
vided and (2) that it is of “acceptable” quality
(see Chapter 7). When there are concerns about
quality, referral can be made to the state’s peer
review mechanism if the matter cannot be
resolved to the satisfaction of all involved.
Billing for services not actually provided and
other instances of noncompliance with the
contract such as waiving required copayments
are taken seriously by insurers. Although the
problem with billing for services not provided
is obvious, that with waiving of copayment is
perhaps less so. For insurers who base pay-
ments on the UCR method, the copayment is
part of the “usual” fee and often an important
part of the cost-control mechanism as well. If a
dentist has claimed $40 as the usual fee for a
service that has a 20% copayment, the insurer
will pay the dentist $32 and expect the dentist
to collect the remaining $8 from the patient. If
the dentist chooses not to collect this $8, then
the fee is in fact $32, not the $40 claimed, and
the insurer should have paid 80% of $32
instead of 80% of $40. Further, if dentists were
allowed to raise their submitted “usual” fees so
that the fee minus the copayment equaled the
fee that they really wanted, and then simply
forgave the copayment, the cost-controlling
effects of copayment would be lost. Concern
over these billing practices has led to strict laws
in many states, under which these practices are
considered to be felonies. Any dentist dealing
with third-party payment is well advised to
read and understand the rules of participation
and to make a good-faith effort to comply fully
with the terms of the agreement.
Reimbursement of Dentists in Delta
Plans
Because of Delta’s initial close association with
organized dentistry, Delta plans at first used the
7 Financing Dental Care 91
UCR fee-for-service concept almost exclusively,
and this method of payment still dominates.
Under the fee-for-service programs, the way in
which a dentist is reimbursed depends on
whether the dentist is participating or nonpar-
ticipating (often referred to as par and nonpar
dentists) with Delta. A participating dentist is
one who has entered into a contractual agree-
ment to provide care to eligible persons.
Delta plans encourage all dentists to partici-
pate. Those who do generally agree to condi-
tions similar to the following:
●
Agreement to charge Delta-insured patients
their usual and customary fees. The accu-
mulated fees of all participating dentists
form the basis of the UCR fee system. When
a dentist decides to raise the fees charged to
Delta patients, he or she must raise the fees
to all fee-for-service patients. As long as the
new fees are charged to all patients, they
will become the fees that Delta uses for
reimbursement purposes.
●
Acceptance of payment for their services at
an agreed-on percentile (to be described)
as payment in full, which means the dentist
will not assess the patient for any further
charges, other than copayments as speci-
fied by a particular contract.
●
Submission to fee audits by auditors from
Delta, who may check the office records
from time to time. The purpose of these
audits is to ensure that the dentists are
indeed charging their Delta patients the
same fees as they charge their other patients
and that copayments are being properly
billed to the patient.
In the early days of dental insurance, partici-
pating dentists in many Delta plans also agreed
to allow withholding of as much as 5% of the
paid amount. This withheld amount was used by
the new Delta plans to build up sufficient finan-
cial reserves to be able to take on more insurance
risk and in turn to manage more business. As
the corporations built up sufficient financial
reserves, the withhold was reduced or eliminated
in many states. Dentists who chose to become
participating dentists agreed to the withhold
because they supported the idea of developing a
form of payment for dental care that they felt rep-
resented their interests and in which they had
some voice. In addition, the prospect of direct,
prompt payment from the insurer for their
92 Dental Practice
services, which greatly reduced bad debts and
collection problems, was considered by many to
be well worth the small amount withheld.
Nonparticipating dentists can also treat
patients covered under Delta UCR plans and be
reimbursed by Delta. Nonparticipating dentists
are usually paid at the 50th percentile of fees,
rather than the 80th or 90th percentile typically
paid to participating dentists. A nonparticipating
dentist also is free to charge the patient any differ-
ence between her fee and the amount paid by
Delta. The incentive for a covered patient to go to
a participating dentist is that the part of the fee
that the patient must pay (i.e., the copayment)
will usually be smaller than would be the case if
the patient visited a nonparticipating dentist.
Percentile Fees
To illustrate how percentiles are applied to den-
tal fees, suppose that in a given area there are
1000 participating dentists who have a range of
fees for a particular service. The percentiles of a
data set divide the total frequency into hun-
dredths, so that the 90th percentile is that value
below which 90% of the observations lie. In this
example, let us assume that the range of fees
charged for the service runs from $40 to $85. If
each of these filed fees is spread out in a cumu-
lative frequency distribution from the lowest to
the highest, the result might be like that shown
100
80th Percentile = $68
90th Percentile = $72
80
distribution of dentists
Cumulative frequency
60
40
20
0
30
Fig. 7-7 Cumulative frequency distribution of hypothetical fees for a given dental service to illustrate the 80th and
90th percentiles.
in Fig. 7-7. About 10% of dentists charge less
than $60 for their service, 50% charge $65 or
less, 80% charge $68 or less, and 90% charge
$72 or less for this particular service. For this
service, therefore, $72 is the 90th percentile fee.
Ten percent of dentists charge more than $72.
When payment on UCR fees is made at the
90th percentile, 90% of the participating den-
tists receive their full fee for the service, and only
10% are paid less than their usual fee. Those
dentists who normally charge $65 receive $65,
those who normally charge $70 receive $70, and
so on up to $72, the 90th percentile. Those who
normally charge more than $72 are paid $72. If
nonparticipating dentists are paid at the 50th
percentile, which in this example is $65, they are
paid whichever is lower, the fee that they actu-
ally charge or $65.
The rationale behind paying at the 80th or
90th percentile is to control payment at the top
end of the scale while paying the vast majority
of dentists (at least 80% or 90%) their full fee.
This approach fits the definition of “custom-
ary.” It is thus a cost-control mechanism usually
written into Delta plan contracts with partici-
pating dentists.
Preauthorization
Another cost-control mechanism that is widely
used by insurers is preauthorization (also called
40 50 60 70 80 90
Fee (dollars)

predetermination, precertification, pretreatment
review, or prior authorization).4 With pre-
authorization, when the costs of treatment are
expected to exceed some limit (usually several
hundred dollars), the dentist is required by
some carriers, and advised by others, to submit
the treatment plan to the insurer for review
before the treatment begins. This review has sev-
eral functions, including certification that the
patient’s insurance covers the planned treatment
and at what level, and a review of the appropri-
ateness of the care itself by a dental consultant
who works for the insurer. These reviews reduce
the cost of care directly, because some treatment
plans are revised after discussion with a consult-
ant. They also reduce it indirectly, because den-
tists soon learn that insurers are unlikely to
allow expensive treatment when less expensive
alternatives appear to be reasonable.
Procedure Codes
Dental procedure codes also were developed in
the early days of dental prepayment. With the
advent of third-party involvement, an unam-
biguous method had to be developed to define
which procedures would be covered and which
would not, as well as to facilitate the accurate
reporting of which services were provided.
There were various mechanisms for developing
and maintaining these codes through the years,
including the ADA’s Code on Dental Procedures
and Nomenclature. A single set of codes was
mandated with the passage of the Health
Insurance Portability and Accountability Act of
1996. The ADA is the designated agency for
maintaining the dental codes and has estab-
lished a Code Revision Committee for this pur-
pose. Revised codes are issued every 2 years.
Open meetings are held for input, and any
interested party may submit requests for code
revisions.3 All dental insurers now use this stan-
dard set of procedure codes.
Blue Cross and Blue Shield Plans
Blue Cross and Blue Shield plans for many years
offered only limited dental coverage as a part
of their hospital-surgical-medical policies.
Initially, this dental coverage was usually lim-
ited only to services provided in a hospital. The
“Blues” showed little enthusiasm for going any
further into dental prepayment on the grounds
that it was a poor insurance risk, but their atti-
7 Financing Dental Care 93
tude changed once dental prepayment was
shown to be feasible.
Blue Cross and Blue Shield dental plans have
adopted many of the cost-control features pio-
neered by Delta plans. Many now use UCR fees
submitted by dentists, either to reimburse the
dentists in the same way Delta does or to estab-
lish fee profiles or fee screens for different geo-
graphic areas as a basis for reimbursement. In
some states, it is difficult to distinguish Blue
Cross and Blue Shield dental plans from Delta
plans in terms of benefits and administration.
As is now the case with Delta plans in some
states, Blue Cross and Blue Shield plans are
active in offering alternative reimbursement
methods such as capitation, including inde-
pendent practice associations (IPAs) and PPOs
to meet the demands for cost reduction from
purchasers. These alternative provider arrange-
ments are described later in this chapter.
FOR-PROFIT DENTAL PLANS
Commercial Insurance Plans
Once it was clear that prepaid dental plans were
viable and that they were likely to be a significant
part of the health insurance market, commercial
insurance companies began to view dental insur-
ance as a potentially profitable area of business.
The fundamental difference between commer-
cial insurance companies and the dental service
corporations is that the commercials operate for
profit. Therefore, it might be expected that com-
mercial insurance carriers would need to charge
higher premiums than would the service corpo-
rations to allow for the profit margin. In practice,
however, this is not necessarily true, for a number
of reasons. Because there are so many different
for-profit dental insurance carriers, collectively
more people have dental insurance from com-
mercial insurance carriers than from any other
type of carrier.
Commercial insurance is often designed as
an indemnity plan, meaning that cash pay-
ments are made to the providers, rather than as
a service benefit plan. This allows the com-
mercial carriers to organize reimbursement dif-
ferently from the way that dental service
corporations usually do. Dentists in most cases
are not paid according to their UCR fees by a
commercial insurance company; rather, the car-
rier develops fee profiles—that is, the carrier
94 Dental Practice
works out the “going rate” for services from the
reported experience of fees in the area—and
dentists are paid at that rate. The amounts paid
can vary from one insurer to another.
MANAGED CARE
Managed care is a term that is in widespread use
but for which there is no precise definition.
The Health Insurance Association of America
defined managed care as follows:
Systems that integrate the financing and delivery of
appropriate health care services to covered individuals by
means of arrangements with selected providers to furnish
a comprehensive set of health-care services to members;
explicit criteria for the selection of health-care providers;
formal programs for ongoing quality assurance and uti-
lization review; and significant financial incentives for
members to use providers and procedures associated with
the plan.31
This definition is a real mouthful, as compli-
cated as managed care itself. Its key elements are
the following:
A comprehensive set of health care services
●
Selected providers
●
Financial incentives to use the selected
●
providers
Simply stated, what has come to be called
managed care is arrangements through which
people receive all or most of their health care
from providers (hospitals, physicians, and
other personnel) who are formally linked to
the organization. The patient’s out-of-pocket
cost is substantially lower than it would be if
care were sought outside of the managed care
organization.
The most common forms of these arrange-
ments are HMOs and PPOs (described later in
this chapter). There are also innumerable
hybrids, with more coming every day. Although
these types of arrangements are not new, the
movement of the medically insured population
to managed care in the 1990s has been on a
massive scale. It was estimated that in 2001
about 93% of all insured individuals in the
United States were enrolled in some type of
managed care plan.32 At the same time, there
was a concerted effort under way by the federal
Centers for Medicare and Medicaid Services to
move Medicaid and Medicare enrollees from
traditional fee-for-service to managed care. The
effect of these trends on medicine has been pro-
found, for managed care has come to dominate
the practicing life of many physicians.
The primary stimulus for the growth of man-
aged care is concern over the seemingly endless
increases in medical treatment costs, which
were noted earlier in this chapter. The wide-
spread hope is that managed care can somehow
help control the costs of medical care. However,
this hope begs the question as to what is the
“correct” amount of care, and it assumes that
there is some way that this can be determined
for each patient. The hopes for cost control also
depend on the assumption that the “correct”
amount of care will be less expensive to provide
than what people would buy outside of man-
aged care.
No one system for organizing care, however,
can be expected to solve all the underlying
conflicts associated with health and health care.
Although health care is sometimes judged
only in terms of life and death, measuring the
worth of a system is more complex. It is more
sensible to look at how the system affects the
quality of life, although the problem that
immediately arises is that modern medicine’s
ability to add comfort and length to life usually
comes at ever-increasing cost. Every dollar
spent on health care is a dollar that is unavail-
able for some other purpose, which means
that there is an implicit trade-off when an indi-
vidual decides to spend money for more health
care rather than for something else. The prob-
lem becomes especially difficult when small
increases in comfort or longevity come at
high dollar cost. These decisions are difficult
enough when made by individuals with their
own money; they are infinitely more difficult
when made in a public forum with collective
funds.
These tensions associated with deciding how
much health care is appropriate, and for how
much money, are driving the rapid evolution in
the financing and delivery of medical care. That
no single approach is going to be a panacea
should be self-evident, because there is no sin-
gle answer to the underlying question of how
much health care is the right amount, and at
what price. In fact, we see that, even as managed
care is rapidly increasing market share, there is a
growing backlash against it. It cannot satisfy
everyone all of the time, and its promise of con-
trolling costs is seen as the reason for its failures

when inevitably some people experience unsat-
isfactory health care outcomes.
Dentistry in Managed Care
Dentistry is inevitably caught up to some extent
in this financing maelstrom that affects medi-
cine. Virtually all of the innovations that have
been and are being tried in medicine are evident
in dentistry. Some of this has occurred because
purchasing groups have demanded the same
kind of system from their dental coverage that
they are using for their medical coverage. Some
has come from entrepreneurs, both inside and
outside dentistry, who see managed care as an
opportunity to move dental practice into the
future, or more crassly as a way to make quick
money.
On the other hand, there are important dif-
ferences between medicine and dentistry that
make it unlikely that managed care will play as
large a role in dentistry as it has in medicine.
The most important difference is that, whereas
about 85% of the population have medical
insurance, only around 50% have coverage for
dental care. Insured patients account for nearly
all of the income of physicians and hospitals. If
large purchasing groups want these providers to
change their practices, physicians and hospitals
are extremely vulnerable. With dentistry, on the
other hand, there are still large numbers of
patients who are not covered by dental insur-
ance, so that dentists, individually and as a
group, are far less susceptible to pressure from
large purchasers.
The difference in governmental involve-
ment in the payment for care is also impor-
tant. For medical care in general, government
funds account for almost one half of all
expenditures, whereas government funds
account for only about 6% of dental expendi-
tures. 57 As government struggles to control
expenditures, medical care costs cannot be
ignored, but dental care costs are relatively
unimportant. Because it controls such a large
portion of medical reimbursement, govern-
ment is in a position to exert an enormous
influence over providers. In dental care, how-
ever, this is not the case. With Medicaid, for
example, with reimbursement levels well
below what many dentists deem reasonable,
dentists can simply refuse to participate with-
out affecting their economic well-being. This
7 Financing Dental Care 95
would not be possible for many practitioners
in medicine.
Health Maintenance Organizations
Although the idea of HMOs is not new, its
implementation was formally promoted with
the passage of the Health Maintenance
Organization Act of 1973 (Public Law 93-222).
This act made federal funds for the develop-
ment of HMOs available under certain condi-
tions. It was intended to provide an acceptable
alternative to the fee-for-service private practice
system and help restrain the costs of care.
One of the principal advantages of HMOs, as
a method of providing health care, lies in their
claim to reduce the cost of care for those
enrolled. These savings are purportedly due to
the greater emphasis on ambulatory care and
consequently on reduced hospital utilization as
well as on close control of costly services.
“Unnecessary” hospitalization, principally for
routine diagnostic tests and minor surgery, is
thereby curtailed. Dental care, however, is almost
exclusively ambulatory care, because few dental
procedures require inpatient hospitalization.
The major advantage of the HMO concept in
reducing hospitalization, therefore, has little
application to dentistry, but the close monitoring
of utilization emphasized in HMOs is relevant.
An HMO was defined in the 1973 act as “a
legal entity which provides a prescribed range of
health services . . . to each individual who has
enrolled in the organization in return for a pre-
paid, fixed, and uniform payment.”55 Usually,
but not always, an HMO looks like a large group
practice with a number of services available
under one roof. An HMO is described as having
five essential elements: a managing organiza-
tion, a delivery system, an enrolled population,
a benefit package, and a system of financing and
prepayment.39 HMOs use a prepaid capitation
system of financing medical services. Capitation
means that the care provider is paid a fixed sum
on a regular basis, usually monthly, for each
enrolled person, whether or not the enrollee
uses any care in that month.
Enrollment in HMOs grew rapidly, peaking
at 80.8 million in 1999.32 Since that time
enrollment has begun to decline, likely due to
consumer resistance to what was seen as restric-
tive access to some services. The decline in
HMO enrollments have been more than
96 Dental Practice
balanced by rapid growth in PPOs and point-of-
service arrangements (both to be described
later).
Dental Personnel in Health Maintenance
Organizations
Only a small proportion of HMOs offer dental
services. When dental services are offered, they
are financed through (1) the primary capitation
premium, (2) a separate premium, or (3) a fee
for service. When included, the dental care itself
can be provided in an HMO according to one of
four basic organizational models:
Staff model: Dentists, dental hygienists, and
dental assistants are salaried employees of
the HMO. The staff model is the only one
of the four modes that affects auxiliary per-
sonnel directly, because in the other three,
the terms of their employment in dental
practices do not differ from those in tradi-
tional private practices.
Group model: The HMO contracts directly
with a group practice, partnership, or
corporation for the provision of dental
services. The group receives a regular capi-
tation premium from the HMO.
IPA: The IPA is an association of independent
dentists (or physicians in medical practice)
that develops its own management and fis-
cal structure for the treatment of patients
enrolled in an HMO. An IPA is thus not a
different form of practice but instead a
legal arrangement through which individ-
ual dental offices can participate as
providers to groups of patients who are
enrolled in HMOs. Dentists continue to
practice in their own offices. The IPA
receives its capitation premium from the
HMO (or other prepayment agency) and
in turn reimburses the individual dentists
on either a modified fee-for-service basis
or a capitation basis.
Capitated network or direct contract model: The
network is similar to the IPA, except that
the HMO contracts directly with the indi-
vidual provider for provision of services.
This is the most common form of capita-
tion arrangement in dentistry. Dental
insurers who wish to offer a capitation
product recruit and contract with dental
offices that are willing to have patients
assigned to them.
Assumption of Risk
The concept of assumption of (financial) risk is
important in health care. In the case of patients
who pay for their own care, the situation is
uncomplicated: if the patient accepts the treat-
ment proposed by the dentist, the patient is
responsible for the necessary payment. With the
advent of traditional fee-for-service insurance,
the insurance companies typically agreed to
assume the financial risk. In this arrangement,
there are a set of covered services, usually
subject to some copayments and an annual
maximum, but the insurance company is
responsible for paying for the care with the
money it has collected from the premiums. The
insurer carefully rates each group to estimate
how much the group’s care will cost, so that it
can be sure to set the premiums at a level that is
sufficient to cover the costs of care but not so
high that a competitor will make a lower bid. In
any case, with traditional insurance, the insur-
ance company is “at risk” for most excess costs.
Acceptance of this risk is part of what the insurer
is selling.
In principle, one of the main features of
the capitation method is that the risk, previ-
ously assumed by the insurer, is shifted to the
provider. The essence of the capitation system of
payment is that the provider receives a previ-
ously agreed-on sum per patient enrolled,
regardless of whether or not the patient seeks
care. In return, the provider agrees to provide
specified services as necessary for a predeter-
mined period.
Clearly, the concern of the provider is that
the amount of money received (known before a
contract is signed) be sufficient to cover the
services needed (which are unknown, although
they often can be reasonably estimated, espe-
cially for a large group of patients). If the cost
of the services required exceeds the income
received through the contract, the provider
loses. Conversely, if the services required are less
than the income provided by the contract, the
provider gains. It follows that under some con-
tracts there is the potential for undertreatment
and discouragement of service utilization,
which raises concerns about both ethics and the
quality of care received.38
Therefore it is understandable that both the
ADA and individual dentists are cautious about
assumption of risk. Of course, risk is assumed

by an HMO when it establishes its monthly pre-
mium for its enrollees, just as it is assumed by
any insurer in a prepaid care plan. Capitation,
however, brings the concept of assuming risk
directly to the dentist. By the 1990s, features
such as patient copayments and annual maxi-
mums had become common in capitation
plans as ways to reduce the dentist’s risk. These
were and still are standard cost-control mecha-
nisms in fee-for-service plans.
The pressure for innovative approaches to
control the costs of medical care has in turn
caused purchasers to demand, and insurers to
provide, similar approaches for financing dental
care. As a result, capitation plans are a part of
many dental practices, especially when third-
party payment involves a high proportion of
patients. The basis of capitation, as previously
described, is that the contracting provider,
whether an HMO, group practice, IPA, or indi-
vidual dentist, receives a fixed sum, usually on a
monthly basis, for each eligible patient. The
money is paid regardless of whether patients uti-
lize care. In return, the patient is entitled to
receive covered services that are needed. As of
2002, the National Association of Dental Plans
estimated that about 23.5 million individuals
were enrolled in dental HMOs (sometimes
referred to as DHMOs).41 Enrollment in DHMOs
has actually declined over the past 10 years.
Preferred Provider Organizations
PPOs, along with HMOs, are one of the main
managed care arrangements and the one that is
growing most rapidly. PPOs typically involve
contracts between insurers and a number of
practitioners who agree to provide specific serv-
ices for fees that are lower than the average
for the area. Again following the pattern
established in medicine, dental insurers have
embraced the idea of selectively directing
patients to specific providers (the preferred
providers in a PPO) who have agreed to provide
care to the insured group on a fee-for-service
basis but at fees that are significantly lower than
the usual fees for the area. The contracting
dentists often agree to participate at the lower-
than-usual fees to attract additional patients to
their practices. Competition for patients is the
driving force behind the willingness of some
providers to discount their fees for PPO
patients; clinicians who have ample demand for
7 Financing Dental Care 97
their services at their usual fees, if these usual
fees are higher than those required by the PPO,
are not likely to be interested in a PPO agree-
ment. PPOs differ from HMOs in that they are
fee-for-service plans, so in PPOs a beneficiary
can go to any participating provider for any cov-
ered service, because payment is made only
when care is provided. By 2004, approximately
112 million Americans had medical coverage
through PPOs.1 Just as the popularity of med-
ical PPOs has increased, PPO arrangements
have grown rapidly in dentistry in the past
decade. The National Association of Dental
Plans estimated that dental PPO enrollment in
1999 was 65 million individuals nationwide.41
Most PPOs (both medical and dental) allow
patients to go to providers that are outside of
the PPO panel. However, to encourage use of
PPO providers, and thus to maintain the
expected cost savings from the use of lower-fee
providers, patients receiving care outside of the
network are usually required to pay for a larger
part of their care. With the continuing push to
control the cost of health care, some PPOs have
now come into being that pay nothing for out-
of-network care (except for emergency care).
This form of PPO is usually referred to as an
exclusive provider organization.
Point-of-Service Plans
Point-of-service (POS) plans are managed care
plans that allow enrollees to receive some of
their care, if they wish, from providers who are
outside of the managed care providers. For this
feature, people who choose to receive care out-
side of the panel pay a larger part of the costs of
their care. The recent increase in enrollment in
POS plans indicates that many individuals are
willing to pay extra for their health insurance
to have the increased flexibility that these
plans offer over more restrictive managed care
arrangements.
Concerns Regarding Managed Care
For some, the primary concern with capitation
is that it might encourage undertreatment.
Under “pure” capitation, the dentist receives
the same payment whether or not treatment is
provided, which leads some to argue that this
will encourage undertreatment and neglect.
Others argue that this is a virtue of capitation,
because the dentist is assured a predictable
98 Dental Practice
income and is thus able to make decisions
about treatment without worrying about daily
revenues if treatment need is low. Many think
that the fee-for-service system, in which den-
tists are paid only if they find treatment to pro-
vide, has a high potential for producing
overtreatment. They see this risk as even greater
in the current era of lower disease levels. PPOs
may also encourage overtreatment because the
agreed-on fees are discounted, which thus pro-
vides incentive to provide multiple services per
visit to make each patient visit more economi-
cally worthwhile for the practice. All of these
concerns have led to increasing pressure on
insurers to develop ways to monitor the quality
and quantity of care. Purchasers and individual
patients need to be assured that the care they
pay for is appropriate and of acceptable quality,
regardless of the way for which it is paid. To
assure purchasers that the quality of care is high
and the patterns of care provided are reason-
able, some insurers are conducting increasingly
sophisticated analyses of claims data to detect
patterns that could be signs of substandard or
fraudulent care. In this way, it is possible to
focus most of the more expensive personal
attention on the providers who are most likely
to be providing care in ways that fall outside
the patterns covered by insurance (also see
Quality Assurance in Chapter 6).
DIRECT REIMBURSEMENT
Direct reimbursement is a form of payment for
dental care that has existed informally for a
long time. It continues to be promoted by the
ADA as an alternative to the more common
forms of dental insurance.6 Direct reimburse-
ment involves an agreement between an
employer and its employees in which the
employer agrees to reimburse the employees
for some part of their expenses for dental care.
Employees can go for care to any dentists they
choose. The patient is responsible for paying
the dentist, and the dentist has no responsibil-
ity to the insurer for such things as scope of
covered services or limits on frequency of serv-
ices. All treatment decisions are made by the
patient and the dentist in a traditional two-
party manner. After treatment has been pro-
vided and paid for, the patient takes the receipt
to the employer and is reimbursed for these
expenses according to the rules of the agree-
ment. Reimbursement is usually on a percent-
age basis, and annual limits are common.
The ADA likes direct reimbursement because
it keeps third parties out of the decisions on
which services to provide, how frequently they
can be provided, what the fee will be, and which
dentists will provide them. It is also argued that
direct reimbursement minimizes administrative
costs, although the employer, or a hired admin-
istrator, still must process these reimbursements
and keep track of annual limits.
Groups accustomed to the more conven-
tional forms of third-party dental insurance
have not readily embraced direct reimburse-
ment because they have come to expect and
value such things as direct payment from the
insurer to the dentist, so that patients face fewer
out-of-pocket expenses. They also expect the
insurer to play an active role in ensuring that the
type and quantity of services provided are rea-
sonable and that the quality of care is accept-
able. Direct reimbursement purposely attempts
to keep third parties out of these areas, but for
many purchasers the third-party involvement is
an important part of what they expect from den-
tal insurance. In any event, direct reimburse-
ment has not become a major method of dental
prepayment.
DISCOUNT DENTAL PLANS
In an attempt to find a way to capture markets
beyond the traditional large groups, especially
the individual market, a form of dental bene-
fits that really is not properly called prepay-
ment or insurance has arisen. These discount
dental plans arise when carriers develop pan-
els of dentists who agree to lower-than-aver-
age or discounted fees, similar to PPO panels,
and agree to charge their low fees to patients
who present a discount card. The carrier
charges the patient a small monthly fee for the
discount card. The major difference from
other forms of coverage is that the patient is
responsible for 100% of the discounted fee.
What the monthly fee for the discount card is
buying for the patient is access to a panel of
dentists who have agreed to treat the patient at
a discounted fee. This is a rapidly evolving
product, and its long-term impact is difficult
to predict.

ADMINISTRATIVE SERVICES ONLY
In addition to conventional insurance coverage,
in which the insurer is at risk for the costs of
care, insurers are increasingly providing for pur-
chasers a service known as administrative services
only (ASO). The distinguishing feature of an
ASO contract is that the purchaser of the con-
tract is at risk for the costs of care rather than the
insurer. The purchaser pays a periodic fee that
covers all of the normal administrative services
associated with insurance, such as actuarial
services, claims processing, preauthorization,
posttreatment reviews, and processing of pay-
ments to providers. Virtually all of the types of
payments to dentists that have been described,
in which the insurer is usually at risk, can be
managed on an ASO basis. Whether the insur-
ance company or the purchaser is at risk does
not affect the way the plan appears to the
patient or the dentist. ASO contracts are popu-
lar with large groups, because the groups do not
have to hand over the large sums of money
needed for payment to the insurance company
up front. Instead, the purchasers retain control
over the funds until the time payment is actu-
ally made. The earnings on large amounts of
cash, even if held for relatively short periods of
time, can be considerable and therefore effec-
tively reduce the cost of the insurance to the
purchaser. Although insurance companies han-
dle much of the ASO business, companies
called third-party administrators have arisen
that do no insuring at all. Third-party adminis-
trators handle only the administrative end of
insurance, leaving responsibility for the funds
to pay claims, and therefore the insurance risk,
in the hands of the group.
MEDICAL SAVINGS ACCOUNTS,
HEALTH SAVINGS ACCOUNTS, AND
FLEXIBLE SAVINGS ACCOUNTS
Medical savings accounts and, more recently,
health savings accounts are another attempt to
control the continually rising expenditures for
health care. Both of these allow a person to
establish and add to a special savings account,
protected from taxes, to be used as needed to
cover medical expenses.29,69 These accounts are
meant to cover most small and often discre-
tionary medical expenses and can be established
7 Financing Dental Care 99
only in combination with a high-deductible
insurance policy that covers the more expensive
and infrequent expenses. The theory is that
when individual patients are made responsible
for and thus more aware of the actual cost of
routine medical expenses, they will be more pru-
dent users of care. Use of the high-deductible
insurance policy would be reserved for those
infrequent and high-cost needs that more ide-
ally fit insurance principles. It is too early to say
whether these types of accounts will be widely
used or whether they will be effective in control-
ling the costs of care. Nevertheless, their recent
development is further evidence of the high level
of interest in finding a way to control the costs of
health care. Flexible savings accounts are some-
what different, in that they allow employers to
set up for their employees accounts into which
employees make contributions that are not sub-
ject to income tax. These funds can then be used
during the tax year for qualifying health care
expenses that are not covered by insurance. They
are different from medical savings accounts and
health savings accounts in that they are not
required to be created in conjunction with a
high-deductible insurance policy, and any funds
in the account not used for medical care in the
year are forfeited by the employee, so the
employee must carefully plan how much to have
placed into such an account.68 It is too early to
know whether these mechanisms, in fact, will
have a significant effect on use of medical or
dental care.
FORCES AFFECTING THE DESIGN
OF THIRD-PARTY DENTAL CARE
PROGRAMS
Most mechanisms for controlling the costs of
medical care also affect the way that dental care
is provided and financed. Both HMOs and PPOs
include substantial financial incentives to
receive care from a participating provider. Both
lower out-of-pocket payments and a wider range
of covered services are common methods to
encourage beneficiaries to choose managed care
options. Even though the many forms of insur-
ance options can seem bewilderingly complex,
the underlying forces are straightforward and
will always be present. Purchasing groups want
to buy sufficiently easy and convenient access to
care, at the lowest possible price. For some
100 Dental Practice
groups, the higher cost of wider access is worth
higher premiums; for other groups it is not. In a
growing number of cases, the cost of acceptable
access is more than an employer can afford, and
employees are increasingly being asked to pay a
share of the premiums. In some cases, employ-
ees are required to pay the entire premium, and
in these cases the coverage is voluntary. The only
benefit to the employee in this case is the ability
to buy insurance coverage through a group that
might not otherwise be available as individual
coverage. The continual pursuit by these groups
of the best balance between access to care and
cost will continue to put pressure on providers
to keep costs unber control. To many dentists
the expression cost control is synonymous with
harassment, red tape, and poor quality of care.
However, appropriate methods of cost control
do not demand the use of inferior materials or
techniques. Instead, cost control should be
based on the concepts of evidence and cost effec-
tiveness: that is, how can a purchasing group
best spend the available money to gain maxi-
mum dental health benefits for its members?
Most dental practices have a vital stake in the
continued economic health of the third-party
payment system because it represents a substan-
tial share of their income. At the same time, pur-
chasers of care are taking increasing notice of the
growing cost to them of providing dental insur-
ance.10,24,43 The dental insurance companies are
then on notice that they must keep the costs of
the plans that they offer under control, which in
turn affects dentists’ incomes. A number of such
mechanisms have been described and are in
common use; others are continually under
development. If cost controls are not routinely
and successfully incorporated, individual dental
plans will simply not succeed in the market-
place. The challenge is to find ways of keeping
the costs of dental care within the range that pur-
chasers are willing to pay, while at the same time
providing a level of care and access to providers
that both dentists and patients find acceptable.
Although dentists may have difficulty accepting
the idea that not every patient should have all of
the care that money can buy, purchasers of care
for large groups are increasingly unwilling or
unable to pay the insurance premiums needed
to support open-ended benefits.
Although the cost of dental care is much
smaller than the cost of medical care, dental care
is nevertheless subject to the same kinds of
pressure as is medical care. Although the mecha-
nisms employed are numerous and are con-
stantly evolving, and can thus be confusing and
frustrating to providers and patients alike, the
underlying principles are really quite simple. The
challenge for those who design dental insurance
products is to find the best balance between
access and price. At one extreme, if insurance cov-
erage will pay for whatever a patient and dentist
decide is to be done, with few and small patient
copayments, the premiums required will tend to
be relatively high. Less expensive will be a plan
that limits payments only to dentists who have
agreed to provide services at low or discounted
fees (i.e., a PPO) or one that requires substantial
deductibles or patient copayments. Perhaps least
expensive of all would be a plan that provides the
beneficiary with a discount card which, when pre-
sented to a participating dentist, assures that the
dentist will charge discounted fees, but these fees
will be paid entirely by the patient. The number
of variations is endless, and the resulting continu-
ing dance of product designs is an attempt by the
various insurance companies to match this bal-
ance between access and cost to create products
that will be attractive to customers. This balance
can be especially critical for dental insurance
because, unlike with medical insurance, the risks
of going without dental insurance are not large.
Therefore the challenge for dental insurance com-
panies is not only to meet the competition posed
by other insurers but also to meet the challenge of
the customer’s deciding to go forward with no
dental insurance at all. This concept is so impor-
tant that it bears repeating. A prepayment system
for dental care that cannot continue to provide to
groups a level of coverage (access) that it wants at
a cost that is acceptable is at risk of having the
group decide that it can do without dental cover-
age altogether. Both patients and dentists would
lose in such a situation. Without help to pay for
the care, fewer patients would receive care, and
dentists’ incomes would decrease.
Third-party plans do not remove the cost bar-
rier to dental care; they merely change its nature.
The amount of care a plan can finance is still
finite; the object of controls is to try to use the
available financing to best advantage.9 The more
that dentists are able to accept this philosophy,
the better they will be able to work with pur-
chasers and administrators to devise mutually

acceptable methods of cost control. The contin-
ual pushes and pulls of the prepayment market-
place are not there to harass dentists and patients,
but instead are a manifestation of the unrelenting
pressures of the marketplace to stay within the
range of an acceptable access-price balance.
PUBLIC FINANCING OF HEALTH CARE
The federal government has been involved in
the direct financing of health care almost from
the founding of the United States. Congress in
1798 established the Marine Hospital Fund, the
forerunner of the U.S. Public Health Service, to
provide medical care for merchant seamen. The
federal government gradually accepted respon-
sibility for providing health care to other
groups: the care received by military and Coast
Guard personnel, American Indians, Alaska
Natives, and inmates of federal penitentiaries is
financed with federal funds and often provided
at federal facilities. This limited and carefully
defined role of the federal government was seen
for a long time as its right and proper function
in health care provision.
The relation between the various levels of
government in the United States was perma-
nently changed in 1935 with the passage of the
first Social Security Act. This act was passed
in the midst of the Great Depression, when
unprecedented problems were caused by mass
unemployment and widespread poverty. The act
created a system financed from compulsory
employee-employer contributions to provide
income maintenance for the elderly. The Old
Age Insurance (OAI) provisions of the original
act of 1935 became extended to the Old Age and
Survivors Insurance (OASI) in 1939 and then to
the Old Age, Survivors, and Disability Insurance
(OASDI) in 1960.53 All provisions of the Social
Security system until then were related to
income security, rather than to the financing of
health care. In addition, public welfare pay-
ments at that time were made directly to the
recipients only. These payments were so low that
most individuals could afford only limited
emergency health care, and the choice was left to
the recipient about whether to buy health care
or something else. It is perhaps not surprising
that recipients of public welfare tended to seek
health care only when they perceived themselves
or a member of their family to be seriously ill.
7 Financing Dental Care 101
The Social Security Act of 1935 provided no
funds expressly for the provision of health care.
During the Great Depression, however, people’s
inability to purchase health care in the tradi-
tional way was recognized as a major social
problem. A system of grants-in-aid was thus
developed as a method of using federal finances
for needed health care services without disturb-
ing the traditional federal-state separation.
Grants-in-aid were federal funds allocated to
the states according to specified formulas. To
receive these grants, the states had to expend
their own funds for the same objectives as those
supported by the grant-in-aid, often in the ratio
of $1 from state or local sources to $2 from fed-
eral sources.25 Grants-in-aid during this period
were available only for support of specific cate-
gories of needy individuals, such as the blind,
dependent children, permanently and totally
disabled individuals, and the aged.
A significant change in methods of federal
financing for health care came with the passage
of the Kerr-Mills bill in 1960. This legislation,
supported by both the ADA and the American
Medical Association, linked health care needs to
the general welfare of the aged indigent by a
program known as Medical Assistance to the
Aged. Although the effects of this program were
relatively disappointing,53 the Kerr-Mills bill
introduced the use of vendor payments, mean-
ing payments directly to those who provided
service rather than to the recipients of care. This
procedure ensured that allocated funds could
be used only for health care.
Growing public awareness in the early 1960s
of the problems of poverty and ill health set the
stage for the 1965 amendments to the Social
Security Act. These amendments were in their
own way as landmark a piece of legislation as the
original act 30 years earlier. Title XVIII, known as
Medicare, provided for the receipt of health care
services by all persons aged 65 and over, regard-
less of their ability to pay, and Title XIX, known as
Medicaid, was intended to bring access to health
care to the indigent and medically indigent seg-
ments of the population. The term medically indi-
gent refers to those who are not dependent on
public welfare to meet the basic necessities of life
but who do not have sufficient income to pur-
chase health care through the usual private prac-
tice channels. (This concept is meaningless, of
course, because costly new developments in the
102 Dental Practice
diagnosis and treatment of previously untreat-
able diseases can make anyone but the super-rich
medically indigent should they be unfortunate
enough to get the wrong disease.)
In 1997 the Social Security Act was further
amended through Title XXI, which created a
State Children’s Health Insurance Program
(SCHIP). SCHIP provides federal funds to states
and, like Medicaid, requires that the states
also use some of their own funds to provide
payment for health care for children in fami-
lies whose income is too high to qualify for
Medicaid but still too low to be able to afford
health insurance.
Public Expenditures for Dental Care
By 2002 just over 6% of all dental expendi-
tures were from public funds, compared with
more than 46% of total health expenditures.57
Fig. 7-8 shows the proportions of public and
various types of private payments for different
areas of health care in 2002. It can be seen that
payment for dental care is close to evenly
split between private insurance and out-of-
pocket patient payments. Government, plus
100
80
60
Percent
40
20
0 Both parts contain a highly complex series of
Hospital Physician Drugs Dentist
Government
Other—private
Private insurance
Out of pocket
Fig. 7-8 Proportionate expenditures on various categories
of health services by type of payment in the United States,
2002.57
other sources such as charity, account for the
remaining 6% of dental payments.
The proportion of total public expenditures
on health care services in 2002 that went to den-
tal care was also very small, less than 0.7%.
More than 40% of all public expenditures for
health care went toward hospital care; the other
major areas of public expenditure were physi-
cians’ services, nursing home care, public health
activities, and research.57
North Carolina established the first state den-
tal division in 1918, and many other state-level
dental public health programs developed
between 1935 and 1965. A great variety of dental
care programs were instituted, financed, and
administered by state and local communities
during this period, frequently with the help of
federal monies through grants-in-aid. Many
state-level dental public health programs, focus-
ing on maternal and child health populations,
got their start via such grants-in-aid through
what was then the Children’s Bureau. These pro-
grams vary greatly from state to state. Although
some are strong and active, in many states these
programs are small and inadequately financed.
Medicare
Title XVIII of the Social Security amendments of
1965 is the program known as Medicare. As orig-
inally conceived, it removed financial barriers
for hospital and physician services for persons
age 65 and over, regardless of their financial
means. Medicare also covers some people who
are disabled as well as people with permanent
kidney failure. Expenditures on the Medicare
program in the first few years of operation were
considerably higher than estimated, and it was
not long before some financial constraints were
introduced. By the mid-1970s, Medicare had
two parts: Part A, hospital insurance, and Part B,
voluntary supplemental medical insurance.
service benefits, and both parts also require
some copayment by the individual. Apart from
these copayments, Medicare is financed com-
pletely from Social Security funds.
Medicare was brought into being because the
voluntary health insurance system was unable
to provide adequately for people over age 65.
The health insurance industry must collect pre-
miums sufficient to cover what it must pay out,
and the risk of adverse selection in those over

age 65 is high. In addition, because the income
of persons aged 65 and older is usually consid-
erably less than that of those in the employed
population, they have limited funds to spend
on health care. Hence, there were twin prob-
lems of high health care needs and low income.
The uproar from the health professions that
surrounded Medicare’s birth in 1965 (“social-
ized medicine”) subsided as the public realized
that it filled a necessary gap in the financing of
health care. Data from the website of the Centers
for Medicare and Medicaid Services, the federal
agency that administers Medicare and Medicaid,
show that, in 2002, more than 40.5 million
Americans, about 14.5% of the population,
were enrolled in Medicare. Federal expenditures
for the program were estimated to be approxi-
mately $236 billion in 2002, or $5800 per
enrollee.57 In late 2003 legislation was passed to
add prescription drug benefits to Medicare by
2006. The dental segment of Medicare is limited
to those services requiring hospitalization for
treatment, usually surgical treatment for frac-
tures and oral cancer, and hence constitutes a
negligible part of the program.
Medicaid
Medicaid, Title XIX of the Social Security
amendments of 1965, differs from Medicare in
several important ways. Whereas Medicare is
funded wholly from federal funds, Medicaid
costs are shared jointly by the federal and state
160
Actual dollars
140 Real dollars
120
Billions of dollars
100
80
60
40
20
0
1972 1980
Fig. 7-9 Total Medicaid expenditures in actual dollars and adjusted to constant 1972 dollars (real dollars) in the
United States, selected years, 1972–98.52,65,66
7 Financing Dental Care 103
governments. In 2004 the federal government
provided 53%–80% of the funds used by each
state.77 Federal allocations are made according
to a formula based on the ratio of the state’s per
capita income to the national per capita
income.74 The original intent of Medicaid was
to provide funds to meet the health care needs
of all indigent and medically indigent persons.
Eligibility standards vary widely from state to
state, as do the expenditures on authorized serv-
ices. For example, in 1998 the average Medicaid
expenditure per recipient nationally was about
$4300, but in some states it was almost $9000
and in others just over $2000.60 Medicaid is a
major source of health insurance for children.
In 1998 almost 20% of children in the United
States were insured by Medicaid.58
Expenditures for the overall Medicaid program
have shown a steady growth through the decades,
as indicated by Fig. 7-9. Even after adjustment for
inflation, the pattern shows a steady increase over
time. Medicaid expenditures for dental care, how-
ever, follow a quite different pattern, as shown in
Fig. 7-10. Real (adjusted for inflation) dollar
expenditures for dental care have changed rela-
tively little since the early 1970s.52,65,66
A pattern of a relative decline in dental
expenditures within Medicaid is demonstrated
in Fig. 7-11, which shows that the proportion of
the total Medicaid budget going to dental care
has fallen steadily from nearly 3% in 1972 to
well under 1% in the late 1990s. Small as this
1986 1988 1990 1992 1994 1996 1998
Year
104 Dental Practice

1200
Actual dollars
1000 Real dollars

Millions of dollars
800

600

400

200

0
1972 1980 1986 1988 1990 1992 1994 1996

Year
Fig. 7-10 Medicaid expenditures for dental care in actual dollars and adjusted to constant 1972 dollars (real dollars)
in the United States, selected years, 1972-97.52,65,66

2.5

2
Percent

1.5

0.5

0
1972 1980 1986 1988 1990 1992 1994 1996

Year
Fig. 7-11 Medicaid expenditures for dental care as a percentage of total Medicaid expenditures in the United States,
selected years, 1972-97.52,65,66

fraction is, it still represents the bulk of public
expenditures for dental care. This decline is
made more severe by the rise in the number of
recipients of dental services through this time
from 2.4 million in 1972 to well over 5 million
in 1998.52,65,66 The result is that the expendi-
ture for dental care per dental recipient fell
throughout the period, as shown in Fig. 7-12.
Expressed in constant 1972 dollars, payments
dropped from nearly $71 per recipient in 1972
to $45 in 1997. In the mid and late 1990s, well
under 20% of Medicaid recipients received den-
tal care under the program.
To qualify for the federal government’s share
of Medicaid financing, every state Medicaid pro-
gram is required to cover a set of basic services
for all children receiving federally supported
financial assistance. In addition, amendments
to the Medicaid program instituted in 1968
required that states offer early and periodic
screening, diagnosis, and treatment (the EPSDT
program) to needy children through age 20.
Medical, dental, vision, and hearing services are
mandatory under the EPSDT program.
Unfortunately, the EPSDT program contin-
ues to be a long way from fulfilling its promise.
Of slightly more than 21 million children under
the age of 21 who were eligible for EPSDT serv-
ices in 1993, just over 4 million (under 20%)
received preventive dental services.64 With the
exception of some relatively small demonstra-
tion projects to increase access, very little has

200
Actual dollars
Real dollars
160
120
Dollars
80
40
0
1972 1980 1986
Fig. 7-12 Medicaid expenditures for dental care per dental recipient, in actual dollars and adjusted to constant 1972
dollars (real dollars) in the United States, selected years, 1972-98.52,65,66
improved over the past decade.21 National sta-
tistics continue to show that only 20%-30% of
Medicaid-enrolled children receive any dental
care in a given year.64,70,71
Although Medicaid has reached a large num-
ber of people, there clearly are gaps. Despite the
fact that well over 40 million people in the
United States are without health insurance,32
there have been and continue to be efforts to
limit Medicaid expenditures.14 The economic
recessions of the early twenty-first century have
sharply increased the number of people eligible
for Medicaid, and because this happened during
periods of rapidly increasing medical care costs,
the higher costs of the Medicaid program were
seen as excessive by many states. As a result,
some states cut back on eligibility, reducing the
availability of services and the levels of payment
to providers. Unfortunately, dental services are
often included among the first of these cutbacks,
and Medicaid-funded services for adults have
been especially hard hit. Many dentists, frus-
trated by rapidly changing eligibility standards
for prospective patients, reductions in available
services, changes in percentile fees paid, and
delays in payment for services rendered, have
refused to treat patients under Medicaid.
The future of Medicaid at the beginning of
the twenty-first century remains clouded. For
one thing, the pressure to reduce government
spending at both the federal and state levels is
relentless. Medicaid is a prime target for reduc-
*Reference 11–13,17,20,35,40,67,70,71,75,76.
7 Financing Dental Care 105
1988 1990 1992 1994 1996 1998
Year
tions, partly because it does not have a vocal
constituency. Although the over-65 population
is a powerful, articulate, and politically potent
force in support of Medicare, the Medicaid-
eligible population is not such an advocate.
Although the federal government continues to
push responsibility for Medicaid toward the
states, the states already feel overburdened by
Medicaid costs and are resisting. Whatever
the outcome, the most likely losers are the
Medicaid recipients, who are threatened with
loss of access to health services provided by pri-
vate practitioners.
The philosophy of shifting social welfare pro-
grams from the federal government to the states
will cause continuing loss of needed services if
funding is not also made available to already
stretched state budgets. State governments, unlike
the federal government, are unable to operate at a
deficit. If tax revenues and other sources of funds
are not sufficient to meet all of the budget needs,
programs simply must be reduced or eliminated.
The development of block grants, in which previ-
ously categorical federal funds (evolved from the
grant-in-aid days) are lumped together to be allo-
cated to specified programs at a state’s discretion,
is causing difficulties for dentistry. The total sum
of federal funds received by the state is reduced,
and there are heavy political pressures to use the
funds for health-related purposes other than den-
tal care. The immediate future for traditional pub-
lic health programs does not look optimistic,
although philosophies may change if large
numbers of people are unable to get the care
106 Dental Practice
they need. Although there have been innovative
small-scale demonstration programs in some
states that show promise for overcoming some of
the access problems for the Medicaid population,
the long-term success of these and other pro-
grams will ultimately depend on sufficient fund-
ing. There is simply no way to provide dental care,
or anything else, without adequate funds.
On the positive side, the nearly $3.7 billion
paid by Medicaid for dental services in 2002,
although far short of what was needed, has still
allowed dentists to treat many patients who
would otherwise not have received care.57 It
should also be remembered that numerous pub-
lic and philanthropic dental programs derive a
substantial portion of their operating revenues
by billing Medicaid for services that they provide
to enrolled individuals, and in this way Medicaid
plays a key part in sustaining and enlarging these
safety net programs. Nevertheless, it is troubling
that virtually all state Medicaid programs are out
of compliance with the requirements for
Medicaid and EPSDT, that this noncompliance is
well known by all involved parties,54 and that lit-
tle enforcement is carried out. A vocal dental
constituency is needed to force action.
In an effort to help control the costs of both
Medicare and Medicaid, government has made
a major effort to encourage enrollment in man-
aged care plans. Although there has been some
success in moving beneficiaries to managed
care, especially in Medicaid, for which there is
no other option in some states, it remains to be
seen whether or not costs are actually controlled
in the long run and whether access and other
quality indicators will be at satisfactory levels.
State Children’s Health Insurance
Program
SCHIP, enacted in 1997 under Title XXI of the
Social Security Act, is intended to encourage states
to provide health coverage to many of the more
than 10 million uninsured children in the United
States. SCHIP is intended for children whose fam-
ilies have incomes that are above those for
Medicaid but are too low to enable them to afford
conventional health insurance. SCHIP covers
children in families who have incomes up to at
least 200% of the federal poverty level (a federally
defined level of income that defines poverty for
government purposes [see Chapter 2]), although
states have some flexibility to set higher limits to
include more children. By 2003 about 5.8 million
children in the United States were enrolled in
SCHIP, a bit over 7% of the child population of
the country and about one half of the uninsured
children that SCHIP initially intended to reach.59
Because the states have more flexibility in the
design of their SCHIP programs than is the case
for Medicaid, the programs can differ markedly
from one state to another. They can vary from a
simple expansion of the state’s Medicaid program
with no difference from the Medicaid program at
all to a completely separate program with a differ-
ent set of rules. These separate SCHIP programs
may require patient copayments, monthly premi-
ums, and annual payment limits, none of which
is permitted under Medicaid.
Other Programs of Public Financing
for Dental Care
The Indian Health Service (IHS) is responsible
for medical and dental care for over 1.6 million
American Indians and Alaska Natives who are
members of federally recognized tribes.2 The
IHS provides care through over 230 hospitals
and clinics in 35 states, and employs approxi-
mately 400 full-time dentists and 1400 hygien-
ists and dental assistants.63 The Division of Oral
Health of the IHS is responsible for direct care
through its own clinics and contract care through
private dental offices for a large portion of this
population. Federal funds also are provided for
some tribes to run their own programs. Dentists
who are commissioned officers in the U.S.
Public Health Service are also assigned to pro-
vide dental care for U.S. Coast Guard personnel
and inmates in federal prisons.
Community and migrant health centers are
joint state-federal projects designed to bring pri-
mary and preventive health care to medically
underserved areas throughout the United States
and its territories.61 Many of these centers pro-
vide dental services and preventive education.
A substantial part of the federal Maternal and
Child Health Services block grants (Title V
funds) are also used by individual states for
dental care, and funds are available for dental
care through Head Start for prekindergarten
and kindergarten children from deprived back-
grounds who are otherwise not eligible for
Medicaid. Other programs with federal involve-
ment that have a dental care component are the
Health Care for the Homeless program and the

National Hemophilia Program, which provides
a wide range of services for hemophiliacs. There
also are funds available for individuals with
human immunodeficiency virus infection
under the federal Ryan White CARE Act.62
Rehabilitative care for children born with
cleft lips and palates has long been financed
cooperatively by state funds and federal grants-
in-aid because it was recognized that just about
everybody is “medically indigent” when it
comes to treatment of cleft lip and palate. All
states have some resources available for team
treatment of this condition. Dental personnel
should be aware of resources available in or
near their communities.
Unfortunately, public financing for the den-
tal care of people with other handicapping con-
ditions—for example, those with cerebral palsy,
mental retardation, paraplegia, or quadriplegia
—has never been as forthcoming. Although
some states do have reasonable programs for
the treatment of children with these conditions,
few have any kind of financing available for
their dental treatment when they become
adults. The dental treatment of chronically ill
and homebound adults has also been neglected
almost completely, despite a successful demon-
stration program for providing dental care to
the homebound.73
The program of the Department of Veterans
Affairs (formerly the Veterans Administration,
or VA) provides some dental care to eligible vet-
erans through its inpatient and outpatient facil-
ities nationwide. As previously noted, the
various branches of the military also provide
direct care for active duty personnel, and a vol-
untary dental insurance program, currently
called TRICARE, which usually requires the par-
ticipants to pay part of the cost, is available for
dependents of military personnel. Similar vol-
untary insurance programs are available for mil-
itary retirees and members of the reserve forces
(National Guard). For all of these programs for
other than active duty personnel, care is often
provided through private dental offices, with
payment partially paid according to the insur-
ance coverage.19
National Health Insurance
Although the idea of national health insurance
(NHI) in the United States is not new,15 the fact
that serious proposals for some form of it peri-
7 Financing Dental Care 107
odically resurface testifies to the persistence of
the dual problems of (1) large numbers of peo-
ple who have no insurance, and (2) the unre-
lenting increases in the costs of health care
services.
If NHI is perceived as simply a financing
mechanism without any restructuring of the
care system, however, the rate of cost increases is
not likely to diminish.27,34 Indeed, the rate of
increase in direct expenditures would far exceed
present levels. The characteristics of the system
that have fueled the continuing rise in the pro-
portion of GDP that goes to health care would
be magnified by an additional large infusion of
funds. The trade-offs required to balance need
against costs will present challenges for which
American society seems unprepared.44 This
realization, added to concerns about a balanced
federal budget and strong opposition from
medicine, dentistry, and private health care and
pharmaceutical interests, is responsible for the
hesitancy in enacting NHI.
Although proposals for universal and com-
prehensive publicly financed health insurance
have been consistently swept aside, the record
clearly shows that government involvement in
health care financing has been steadily increas-
ing over the long term. Especially since 1965,
when the federal government got involved in
direct payment for care in a big way with
Medicare and Medicaid, we have seen slow
expansion in the groups covered. Given the rela-
tive success and popularity of these programs,
and recent expansion to include prescription
drugs in Medicare, which covers essentially all
the over-65 population, and the expansion of
the Social Security Act (Title XXI) in 1997 to
include many uninsured children, there is some
level of government-assisted health care cover-
age for virtually all but the working-aged popu-
lation. There remain the dual concerns of, on
the one hand, whether the funding for these
programs is adequate, especially for Medicaid
and the State Children’s Health Insurance
Program, and, on the other hand, whether tax-
payers are willing to support what look to be
ever-growing programs. Further, coverage for
dental services continues to be a small part, at
best, of these government health programs. For
the foreseeable future, most Americans who
receive regular dental care will continue to pay
for it with private insurance or their own funds.
108 Dental Practice

Those unable to pay will continue to be far less 19. Department of Defense, Office of the Assistant
likely to receive regular care. Secretary of Defense. What is TRICARE?, website:
http://www.tricare.osd.mil/whatistricare.cfm. Accessed
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 8 The Dental Workforce
TYPES OF DENTAL PERSONNEL
Dentists
Dental Auxiliaries
SUPPLY OF DENTISTS IN THE UNITED
STATES
Dental Specialists
Distribution of Dentists
Effect of Dental Education on the Supply of
Dentists
State Practice Acts and Dentist
Distribution
The vision of the dental team is one of various
people in dentistry with different roles, func-
tions, and periods of training, all working
together to treat patients.106 Dental team is more
a concept than a precise term, although the den-
tal profession in the United States has long rec-
ognized that several different categories of
personnel are fundamental to the efficient pro-
vision of care. Virtually all dentists employ at
least one nondentist staff person, more than
94% of general practitioners employ at least
one full- or part-time chairside assistant, and
more than 63% employ at least one full- or part-
time hygienist.29
This chapter defines the various types of per-
sonnel involved in the provision of dental serv-
ices and assesses the factors that influence their
supply and distribution.
TYPES OF DENTAL PERSONNEL
Dentists
A dentist is a person who is permitted to practice
dentistry under the laws of the relevant state,
province, territory, or nation. These laws are
intended to ensure that a prospective dentist
has satisfied certain requirements such as
(1) completion of a specified period of profes-
ALLIED DENTAL PERSONNEL IN THE UNITED
STATES
Dental Hygienists
Dental Assistants
Expanded Function Dental Auxiliaries
Dental Laboratory Technicians
Denturists
LEGISLATIVE INFLUENCE ON DENTIST
SUPPLY AND DISTRIBUTION
National Health Service Corps
Subsidies to Dental Schools and Dental Students
sional education in an approved institution,
(2) demonstration of competence, and (3) evi-
dence of satisfactory personal qualities. Dentists
are concerned with the prevention and control
of the diseases of the oral cavity and the treat-
ment of unfavorable conditions resulting from
these diseases or from trauma or inherent mal-
formations. A dentist is legally entitled to diag-
nose and treat patients independently, to
prescribe certain drugs, and to employ and
supervise auxiliary personnel. The mechanisms
for fulfilling these requirements differ among
nations. In the United States and Canada, for
example, professional education is separate
from the additional testing required for licen-
sure. In many other countries, these two func-
tions are combined under the authority of the
educational institutions.
Dental Auxiliaries
Dental auxiliary is a generic term for all persons
who assist the dentist in treating patients. It
includes the categories of dental hygienist,
dental assistant, hygienist or assistant with
expanded functions, dental laboratory techni-
cian, receptionist, and secretary. Auxiliaries
can be classified as operating and nonoperat-
ing,107 depending on whether they carry out any
111
112 Dental Practice
intraoral procedures in the direct treatment of
patients.
With rare exceptions, auxiliaries of all types
operate under varying degrees of supervision
by dentists. Even those auxiliaries who appear
to operate more or less independently, such
as the school dental therapist of New Zealand
(see Chapter 6), work under some degree of
supervision. Defining the extent of supervision
required for various types of dental auxil-
iary can be confusing, because bodies con-
cerned with supervision continue to modify
their stance and definitions. As of 2002, the
American Dental Association (ADA) acknowl-
edged four levels of supervision of allied dental
personnel as shown in Box 8-1.
The ADA policy statement on this issue
declares: “General supervision is not acceptable
to the American Dental Association because it
fails to protect the health of the public.”8 This
issue is important for public health programs
because, without general supervision, it is far
more expensive for dental hygienists to provide
care in schools, nursing homes, and other insti-
tutional settings. Where general supervision is
permitted, dentists in private practice can allow
a hygienist to provide recall prophylactic serv-
ices while the dentist is away from the office.
These policies of the ADA have no direct con-
trol on the practice of dentistry because the reg-
ulation of dental practice in the United States is
determined by state licensing boards, not by the
BOX 8-1 Levels of Supervision of Allied Dental Personnel As Defined by the American Dental Association
in 20028
1. Personal supervision: The dentist is personally
operating on a patient and authorizes the allied dental
personnel to aid treatment by concurrently
performing a supportive procedure.
2. Direct supervision: The dentist is in the dental office or
treatment facility, personally diagnoses the condition to
be treated, personally authorizes the procedures and
remains in the dental office or treatment facility while
procedures are being performed by the allied dental
personnel and, before dismissal of the patient, evaluates
the performance of the allied dental personnel.
3. Indirect supervision: The dentist is in the dental
office or treatment facility, has personally
(Copyright 2002 American Dental Association. Reproduced by permission.)
professional organization. Each state can have
its own definition of supervision requirements
and scope of practice, and indeed there is con-
siderable diversity among states. The moves by
the ADA to limit the scope of auxiliaries’ prac-
tice are occurring as dental hygienists are work-
ing for a greater degree of autonomy, so
conflicts are to be expected.
A dental hygienist is an operating auxiliary
licensed to practice dental hygiene under the
laws of the appropriate state, province, territory,
or nation. In nearly all jurisdictions, to be
licensed, hygienists, like dentists, must satisfy
certain qualifications such as (1) completion of
an approved period of education in an approved
institution (only Alabama permits on-the-job
training of hygienists),81,99 (2) demonstration of
competence, and (3) demonstration of satisfac-
tory personal qualities. Hygienists are recog-
nized auxiliaries in a number of countries, in
which their duties and deployment are essen-
tially similar.62
Dental hygienists have traditionally been
concerned with prophylaxis, the health of the
supporting structures of the teeth, and preven-
tion of further diseases by direct clinical pro-
cedures and by the education of individual
patients and groups. In most places, hygienists
work under the supervision of dentists, either in
private dental practice or in institutional set-
tings such as health departments, nursing
homes, or school dental programs.
diagnosed the condition to be treated, authorizes
the procedures and remains in the dental office or
treatment facility while the procedures are being
performed by the allied dental personnel, and will
evaluate the performance of the allied dental
personnel.
4. General supervision: The dentist is not required to
be in the dental office or treatment facility when the
procedures are being performed by the allied dental
personnel, but has personally diagnosed the
condition to be treated, has personally authorized the
procedures, and will evaluate the performance of the
allied dental personnel.
 8 The Dental Workforce 113

The expanded-function dental auxiliary permitted to treat special population groups,

(EFDA) (sometimes called an expanded-duty usually children, with little direct supervision
dental auxiliary) is a more recent development from a dentist. The extent of their duties varies
among operating auxiliaries in the United from one country to another, as does the degree
States and Canada. An EFDA is usually a dental of supervision required, but all dental nurses
assistant, or a dental hygienist in some cases, and therapists require specific training, licen-
who has received further training in duties sure, and registration. Preventive dental nurses
related to the direct treatment of patients, and therapists are trained in some countries to
although still working under the direct supervi- provide preventive services only, usually in a
sion of a dentist. Not all states in the United school dental service. Because their period of
States recognize EFDAs, and the duties permit- training is shorter than the training for dentists
ted in those that do vary considerably. and their duties are limited, these auxiliaries can
A dental assistant is a nonoperating auxiliary provide preventive services to specified groups at
who assists the dentist or dental hygienist lower cost than can dentists or hygienists.
in treating patients but who is not legally per-
mitted to treat patients independently. Tradi-
SUPPLY OF DENTISTS IN THE UNITED
tionally the dental assistant’s duties include
STATES
immediate chairside assistance in the handling
of dental equipment and materials used by the Table 8-1 shows the dentist/population ratios in
dentist or dental hygienist in treating patients. several countries as of the late 1990s to give a
Voluntary certification programs for dental perspective on the relative availability of dentists
assistants exist in many countries. Certification in the United States. The range is wide, with an
is the process by which a nongovernmental especially large gap between developed and
agency or association grants recognition to an developing countries, and even within the more
individual who has met certain predetermined economically developed countries, the range is
qualifications specified by that agency or associ- considerable. The numbers are given as the
ation.85 However, a dental assistant is not number of dentists per 100,000 population and
required to be legally certified or registered or to as persons per dentist. The 55 dentists per
have completed any particular duration or
amount of education. The vast majority of the
world’s dental assistants are trained on the job. Table 8-1 Number of dentists per 100,000
However, to provide certain services, such as the population for 15 countries at various stages of
exposure of radiographs, a growing number of economic development108
American states require either some form of for-
Dentists per 100,000 Population
mal education or certification. Country Population per Dentist
The dental laboratory technician is a nonoper-
ating auxiliary who fills the prescriptions Sweden 143 700
provided by dentists regarding the extraoral Finland 98 1024
construction and repair of oral appliances. Denmark 92 1090
Denturist is a term applied to those dental labo- Norway 91 1100
Argentina 83 1200
ratory technicians who are permitted in some
France 72 1390
American states, some provinces of Canada,
Switzerland 62 1613
and some other countries to fabricate dentures United States 55 1810
directly for patients without a dentist’s prescrip- Canada 54 1834
tion. These denturists must be licensed. Illegal Spain 40 2525
denturists are also known to operate in other Singapore 29 3500
jurisdictions. The term can have strong political Turkey 21 4668
overtones in jurisdictions where denturists are Thailand 10 9800
trying to achieve legal recognition. India 3 36,538
Dental nurse and dental therapist are more or Cameroon 1 119,200
less synonymous terms that describe an operat- Ethiopia <1 1,200,000
ing auxiliary who in some countries is legally Note: Rounded to the nearest whole number.
114 Dental Practice
100,000 people in the United States in the mid-
1990s are equivalent to 1810 persons per dentist.
Counting dentists and other dental person-
nel is not as straightforward as it might at first
appear. Membership lists from professional
associations and licensing lists are the most
common source of counts, but these are seldom
completely accurate. For example, some dentists
maintain association membership even when
they are retired or otherwise not actively
engaged in professional practice; others are not
members of a professional association. Dentists
can hold a license in more than one jurisdic-
tion, which leads to overcounting. As a result,
one does well to realize that virtually all enu-
merations of dental personnel are estimates and
that, in an attempt to be more precise, the
counts are often qualified as all dentists, active
dentists (those actually engaged in some
activity related to dentistry), or practicing
dentists (which often excludes dentists in full-
time teaching, research, or administrative posi-
tions). Numbers obtained from different
sources therefore can differ because they are
based on different subgroups. This nomencla-
ture is by no means standard and is often not
clearly defined in source documents. Usually
the differences are not of great consequence, but
when interpretations are made within small
geographic areas the differences can be impor-
tant. For example, in a community where there
is a dental school or a government agency that
employs a number of dentists in nonclinical
positions, a count of all dentists for that com-
munity could greatly overestimate the availabil-
ity of dental care.
As of 2000, the ADA estimated that the num-
ber of professionally active dentists in the
United States was about 168,000. Approxi-
mately 5000 of these were in the armed forces
and other federal agencies.21 About 155,200
dentists were in private practice in 2000, a more
than 55% increase since 1975.93
From 1920 until the early 1980s, 1%–3%
of dentists were women,75,89 but since the
early 1980s this percentage has increased. In
1998, over 13% of dentists were women, and
almost one third of dentists who had graduated
within the previous 10 years were women.26 In
1969–70, women constituted only 1.3% of first-
year enrollment in dental schools,54 but by
1980–81 the first-year class was 19.8% female.55
By the early years of the twenty-first century,
dental school enrollments were over 40%
women.14
Not all observers agree on the implications
of the growing proportion of female den-
tists.10,66,71,75,88,90,102,103 Although it is too early
to be sure about trends, there are indications
that women dentists are more likely to practice
part time and to interrupt their practices for an
extended period of time, thus spending fewer
actual hours in practice during a career. Any dif-
ferences between men and women in retire-
ment patterns will also affect productivity, and
it will be several decades yet before these can be
observed. Further, it is likely that the practice
patterns followed by those women in decades
past, when women in the profession were rare,
may be of little help in predicting the future
practice patterns of the women now becoming
dentists. Although any substantial shift in the
average productivity of dentists would affect the
adequacy of the dentist supply, it is at present
not clear how the increasing proportion of
female dentists is affecting productivity.
Not only are the numbers of women increas-
ing, but dentistry is becoming more ethnically
diverse. Although approximately 90% of den-
tists in practice as of 1995 reported themselves
to be white non-Hispanic,25 the picture for den-
tal students indicates a decided shift. At the turn
of the century, about 25% of dental school grad-
uates listed themselves as other than white.23
Foreign-trained dentists, in contrast to for-
eign-trained medical graduates, have never been
present in large numbers in the United States, in
no small part due to difficulty in gaining licen-
sure. Graduation from an accredited U.S. or
Canadian dental school was for a long time
a prerequisite for licensure in most states.
However, rapid population growth, especially
the growth of immigrant communities, is forc-
ing some states to look at more radical ways of
increasing dentist supply. California, for exam-
ple, is considering accrediting certain foreign
dental schools in a bid to attract dentists from
other countries. The future of such policies
remains uncertain, but their very existence cer-
tainly represents a major break with tradition.
This is a rapidly changing area, and up-to-date
information on the details for any particular
state is usually available on the website of the
ADA.12,30

Dental Specialists
The early development of dental specialists was
informal, and such specialists did not require
certification.60 Varying patterns of formal train-
ing and certification developed as each specialty
grew and matured relatively independently.
Examining boards that certified specialty com-
petence came into being, as did specialty
societies, such as the American Academy of
Pedodontics (now Pediatric Dentistry) and the
American Association of Orthodontists, which
maintained educational and experiential quali-
fications for membership. In addition, some
states established specialty licensure follow-
ing examination by the state board of dental
examiners.
Under guidelines originally set by the
ADA House of Delegates and the Council on
Dental Education, and now maintained by
the Commission on Dental Accreditation, exam-
ining boards have been established in nine areas
of specialty practice: dental public health,
endodontics, oral and maxillofacial pathol-
ogy, oral and maxillofacial radiology, oral
and maxillofacial surgery, orthodontics and
dentofacial orthopedics, pediatric dentistry, peri-
odontics, and prosthodontics. Minimum criteria
for those entering a specialty are full-time limita-
tion of practice, plus either the completion of at
least 2 years of approved advanced study or spe-
cialty licensure by a state board. Certification as
a diplomate by one of the specialty boards is not
a prerequisite for limitation of practice. The
stated purpose of specialty boards is to provide
leadership in elevating standards for the practice
of the specialty and, through examination and
certification, to recognize those individuals
who have demonstrated unusual competence.
Numerous additional dental specialty groups are
not officially recognized by the ADA, and the
ADA actively discourages the announcement of
practice limited to any area other than one of the
nine recognized specialties.
Unlike the situation in medicine, in which by
1990 more than 60% of practitioners were
practicing in a specialty outside of primary
care, about 80% of dentists are general practi-
tioners.25,94 Since the early 1970s, the number
of first-year positions in specialty training pro-
grams has remained stable at approximately
1200. More than 50% of all specialists work in
8 The Dental Workforce 115
orthodontics or oral surgery, the two longest-
established specialties.
There has been strong sentiment in dentistry
for some time that a further increase in the num-
ber of specialists would not benefit either the
profession or the public.59 This view was based
on the contention that one of the chronic prob-
lems in the American health care system is
fragmentation, the dispersal of many medical
specialists and the frequent absence of coordi-
nation among them. The growth of General
Practice Residency and Advanced Education in
General Dentistry programs is a reflection of this
emphasis on the general practice of dentistry. As
of 2004 there were just over 1000 General
Practice Residency and 650 Advanced Education
in General Dentistry residency positions.31
Distribution of Dentists
In 2000 there were approximately 60.7 active
dentists per 100,000 people in the United
States.93 These dentists, however, were not
evenly distributed throughout the country, as
seen in Chapter 6 (see Fig. 6-1). This situation is
not unique to dentistry as a health profession
nor to the United States, for it is found wherever
there is relatively free choice of practice
location. Table 8-2 provides data for the five
most favorable and five least favorable states in
terms of dentists relative to the population in
2000. The figures range from 84.7 dentists per
100,000 people in Hawaii to 39.2 per 100,000
in Nevada.93
Table 8-2 The five states with the highest number of
dentists and the five states with the lowest number of
dentists per 100,000 population in the United States,
200093
State Dentists per 100,000 Population
Hawaii 84.7
New York 83.1
Massachusetts 81.2
New Jersey 80.4
Connecticut 79.6
Alabama 43.5
North Carolina 43.1
Arkansas 42.2
Mississippi 39.7
Nevada 39.2
116 Dental Practice
There are a number of reasons for this
uneven distribution of dentists. The first and
most fundamental is the relative freedom a
dentist has in choosing a practice location.
Dentists make this choice much as other peo-
ple do, that is, because of personal preference:
attachment to a home town, presence of good
schools, or convenience to social, cultural, or
recreational facilities.6 Second, the location of
dental schools also influences distribution, and
the 56 American dental schools are located in
only 34 states (plus the District of Columbia
and Puerto Rico). Most dental schools are in
state universities, at which tuition usually is
less for state residents than for out-of-state resi-
dents. A third reason is market response, mean-
ing that the availability of dentists reflects
demand for services. Areas of high income and
education where demand for services is high-
est, such as affluent suburbs, have more den-
tists than do poorer areas. The low number of
dentists in Nevada is largely a reflection of the
exceptionally rapid growth of the population
of that state in the past decade. The dental
school recently opened at the University of
Nevada, Las Vegas, is expected eventually to
help correct some of that imbalance.
Effect of Dental Education on the Supply
of Dentists
Dentists were first enumerated separately in the
1850 census. It listed 2900 dentists serving a
population of 23 million,91 or 12.6 dentists per
100,000 population. With the growth of dental
schools during the latter part of the nineteenth
century, the supply of dentists in 1900 increased
to 39 dentists per 100,000 population. By 1930,
there were 57.7 dentists per 100,000 popula-
tion.98 This steady increase was caused princi-
pally by changes in dental education. Although
in the second half of the nineteenth century
many dentists were still being trained under an
apprenticeship system, proprietary dental
schools grew rapidly in response to demand
(see Chapter 1). The number of dental gradu-
ates continued to grow until the closing of the
last proprietary school in 1929.70
In the United States, the federal government
has no direct jurisdiction over education, and
there are considerable differences among
states in the priority given to education. This is
notably different from most other countries,
where the national government directly deter-
mines how many practitioners, and of what
type, will be produced. For these and related
reasons, accreditation evolved as a voluntary,
self-regulatory means of establishing and main-
taining nationally acceptable standards of edu-
cational quality.83 Accreditation is the process by
which an agency or organization evaluates and
recognizes a program of study or an institution
as meeting certain predetermined qualifications
or standards.84,85 The Commission on Dental
Accreditation of the ADA currently serves as the
accrediting body for dental and auxiliary train-
ing schools and graduate programs in dentistry.
The commission is a broad-based agency of the
ADA; its membership includes auxiliaries,
public members, and students in addition to
dentists.
Enrollment in dental schools is obviously a
prime influence on the future supply of dentists.
During the 1960s and early 1970s, there was
a widely held perception that more dentists
were needed and that a critical shortage was
inevitable if strong actions were not taken.
Although the federal government in the United
States has no direct control over dental educa-
tion, it can provide incentives to increase supply.
During the 1960s and 1970s, incentives were
offered to dental schools to build new facilities
and to increase the number of graduates at exist-
ing dental schools. The results were impressive,
as shown in Fig. 8-1. The increased applications
and enrollments through the 1970s also coin-
cided with the time that the baby-boomer gener-
ation was deciding on careers. Applications to
dental schools reached all-time highs during
this period; the number of applicants per first-
year position was 2.7:1 in 1974 and 1975.
Applications began to decline in 1976; first-year
enrollments began to decline in 1979. The fed-
eral incentives to dental education were reduced
during this period, and the demographic bulge
passed beyond college age.
The low point in applications and enroll-
ments in the late 1980s coincided with a slow
period in the U.S. economy and again with a
public perception that there was an oversupply
of dentists. During this period, dental schools
made a remarkable adjustment in their capacity.
Through a combination of the closing of six
dental schools and the reduction of class size in
most others, the first-year capacity declined

18000
16000
14000
Number of individuals
12000
10000
8000
6000
4000
2000
0
1951 1956
Applicants
Enrollment
Fig. 8-1 Applicants and first-year enrollees in dental schools in the United States, 1951–2003.2,22,31
from its peak of 6301 in 1978 to approximately
4000 by 1990. Since 1990, applications and
enrollments have recovered considerably, with
first-year enrollments at 4618 in 2003, partly
due to the opening of three new dental schools.
By the late 1990s, evidence suggested that the
economic prospects for dentists, relative to
those for physicians, were quite favorable. A
1994 report analyzing the return on educa-
tional investment among several professions
projected that dentistry would provide a higher
rate of return than primary care medicine and a
virtually identical return to specialty medi-
cine.105 A more recent report suggests, perhaps
because of the pressures on physicians from
managed care, that in some parts of the country
dentists average higher incomes than primary
care physicians.36 These favorable reports of
dentists’ economic prospects may have been a
factor in the growing numbers of applicants to
dental schools from the mid-1990s.
Fluctuations in dental school enrollments
take considerable time to show their effect on
the supply of dentists, and overall supply also is
influenced by other factors. First, with approxi-
mately 160,000 dentists in practice in the
United States, a change of a few hundred gradu-
ates in any one year does not make a large dif-
ference overall. Further, a major influence on
the overall numbers is the number of dentists
8 The Dental Workforce 117
1961 1966 1971 1976 1981 1986 1991 1996 2001
Year
retiring in any one year, which is itself a func-
tion of how many dentists graduated 40 or
more years earlier. Choice of retirement age is
highly variable. If demand for care is strong, a
dentist may wait longer to retire than when
there is an ample supply of younger dentists to
take over. Finally, the population growth of the
country is an additional variable. As population
growth accelerates, more and more dentists are
required to keep the supply constant.
The combination of these factors resulted in
a gradual increase in the supply of dentists in
the United States between 1970 and the mid-
1990s, from 47 to 60 dentists per 100,000 pop-
ulation.95,97 Much of this general increase in
the relative number of dentists is the result of
the large number of graduates through the
1970s and most of the 1980s. Virtually all pro-
jections at the end of the century suggested,
however, that the relative supply of dentists was
at its peak and was likely to decline for the next
several decades. This projected decline will be
the product of lower enrollment levels than in
earlier decades, combined with continuing pop-
ulation growth and projected retirement levels
of dentists. It is anticipated that the relative sup-
ply of dentists will decline especially sharply
between 2010 and 2020, when many of the large
cohort of dentists who graduated in the 1970s
and 1980s are expected to retire. By 2020, it is
118 Dental Practice
expected that there will be about 55 dentists per
100,000 population, back to levels of the early
1980s. Whether this anticipated decline in the
relative supply of dentists will be a problem or
not is discussed further in Chapter 9.
State Practice Acts and Dentist
Distribution
The requirement to hold a state license to prac-
tice inhibits the movement of dentists (and
also licensed auxiliaries) from one state to
another.44,65 In addition, it has been suggested
that certain states adopted deliberately restric-
tive policies in their licensing examinations in
an effort to prevent what they saw as too many
dentists, or dentists “of the wrong kind,” from
practicing in the state.44,51,65,70 Results of
state board examinations show a wide disparity
among states in the proportion of applicants
who fail.5,44,56 Dentists in specialty practice
also report difficulty in moving to states that do
not have specialty licenses. In these instances, a
specialist who may not have practiced general
dentistry for many years may be required to take
a clinical examination based on restorative
procedures.
The ADA supports licensure by credentials to
alleviate some of these problems. Under this
concept, dentists who have passed a licensing
examination in a state present their credentials to
another state to which they want to move; if the
credentials meet the criteria, the board grants a
license. The actual process and requirements vary
widely but generally include requirements for
some minimum time in practice and no evi-
dence of existing or pending disciplinary or legal
actions. The ADA website shows that, in 2004, 43
states plus the District of Columbia and Puerto
Rico allowed some form of licensure by creden-
tials.21 Encompassed within this concept is reci-
procity, by which two or more states agree to
honor each others’ licenses.
Views differ on the value of licensure by cre-
dentials. Some say that the existence of individ-
ual state practice acts, and what is seen as
parochial jealousies in their administration, is a
major cause of maldistribution and that the
problem would be greatly alleviated by licen-
sure by credentials. Others argue that licensure
by credentials could make maldistribution
worse, because large numbers of dentists would
then move to desirable locations.
Movement between states has been made
somewhat easier, at least for the young dentist,
by the development of regional examining
boards. There are four regional boards (North-
east, Southern, Central, and Western), and a
dentist passing the clinical licensing examina-
tion in any participating state can apply, usually
within 5 years of the original examination, for
license in any state in the same region without
having to take another clinical examination. By
2001, 41 states and the District of Columbia
were involved in one or more of these four
regional examining boards.12
Whenever licensure and the assessment of
dentists’ competence are mentioned, the topic
of mandatory continuing education as a
requirement for license renewal also arises. If
the competence of a dentist who moves from
one state to another has to be tested, why
should there not also be concern for those who
stay in one place for many years? Although
there is no clear evidence that mandatory con-
tinuing dental education improves dentists’
competence, by the early part of the twenty-first
century, continuing dental education require-
ments were virtually universal for both dentists
and dental hygienists. As is the case with other
regulatory matters, these requirements vary
widely among states and can change rapidly.
ALLIED DENTAL PERSONNEL
IN THE UNITED STATES
Dental Hygienists
In the early twenty-first century there were esti-
mated to be approximately 120,000 registered
dental hygienists in the United States, nearly an
eightfold increase since 1970.32,96 Table 8-3
shows the growth in the number of active
hygienists and in particular the extremely rapid
growth since the early 1970s (see Chapter 1).
Even with this large increase in the number of
hygienists, there are still some concerns about a
shortage.46,61,104 After declines in enrollment
through the late 1980s, roughly parallel to the
enrollment declines in dentistry, dental hygiene
enrollments rebounded by the turn of the cen-
tury to near-record levels. The majority of dental
hygiene programs are in community colleges,
and in 2004 there were a total of 266 programs
in all 50 states, the District of Columbia, and
Puerto Rico.31
 8 The Dental Workforce 119

Table 8-3 Dental hygienist statistics for the United States: selected years, 1950–200331
Active Hygienists per 100 Training Programs
Year Number of Active Hygienists* Active Dentists in Dental Hygiene First-Year Enrollment

1950 3190 4.0 26 862

1955 4160 4.9 33 1100
1960 8800 9.8 37 1440
1965 11,600 12.1 56 2070
1970 15,100 14.8 121 3265
1975 26,900 24.0 174 5337
1980 38,400 30.4 200 5619
1985 55,000 43.0 198 4866
1990 75,000 55.6 202 5419
1995 100,000 64.5 215 5669
2003 120,000 73.3 266 N/A
*Number of active hygienists is an estimate, because of the relative ease of movement into and out of active practice and the frequency of
part-time practice for more than one employer.

The duties of a dental hygienist are similar in
most countries where they are part of the dental
team.62 These duties, which are usually carried
out under the supervision of a dentist, are asso-
ciated with the preventive aspects of dental care:
scaling and polishing teeth, applying fluorides
and other preventive agents, and educating
patients to practice sound dental habits.
Expanded duties for hygienists have been devel-
oped in some states in the United States, where
the training of hygienists is extended to teach
them to carry out additional duties in the dental
office. Since 1975, however, the ADA House of
Delegates has repeatedly gone on record as
being opposed to delegation of expanded func-
tions to hygienists and other auxiliaries,9,18–20
despite research evidence showing that trained
hygienists can perform these duties compe-
tently. (There is a fuller discussion of expanded-
function auxiliaries later in this chapter.)
Outside of the armed services, dental hygiene
is an almost completely female profession. Even
if this trend continues, the traditional passive-
ness of hygienists has changed. Hygienists,
licensed and regulated by state boards of den-
tistry, have shown their dissatisfaction at not hav-
ing a voice in their own licensing, and there
continues to be considerable activity on the part
of hygienists in many states to gain more control
over their profession. Attempts continue, and
some have succeeded, to develop separate licens-
ing boards for dental hygiene, to increase the rep-
resentation of hygienists on examining boards,
to relax supervision requirements, to allow direct
third-party reimbursement to hygienists, to per-
mit expanded functions, and to allow independ-
ent practice.58 Not surprisingly, the ADA is firmly
opposed to these moves, arguing that the only
appropriate role for a hygienist is provision of
care under the supervision of a dentist.8,16,20
Independent Practice
In 1986 Colorado became the first state in the
United States to permit the independent practice
of dental hygiene. In independent practice, the
hygienist selects a site, rents or purchases space,
secures equipment and supplies, and treats
patients directly. The Colorado legislation,
however, did not permit a full range of hygiene
services; a dentist’s supervision was required for
a dental hygienist to take radiographs, remove
live tissue, perform root planing, and inject
local anesthetic.101 As soon as the bill was
signed into law, the ADA filed suit to block
independent practice, but the court ruled that
the ADA had no standing in the case. This ruling
was upheld in appellate court.81
It is difficult to know how many dental
hygienists have established independent prac-
tices in Colorado, because the law does not
require them to register that fact. Nevertheless,
as of 1998, the number was thought to be fewer
than 20.35 The costs of establishing and main-
taining an office, the limited scope of services
permitted, and the reluctance of insurers
to reimburse hygienists for services appear to
120 Dental Practice
be major barriers to further development,81
even though by 1997 insurers in Colorado were
required to reimburse dental hygienists for cov-
ered services. The limited evidence from
Colorado, and from an experiment in inde-
pendent practice in California, indicates that
independent dental hygiene practices compare
favorably to dental offices on several measures
of practice quality.35,52,77
The future of independent practice for
hygienists remains uncertain, but the overall
trend seems to be a slow expansion of the
autonomy of dental hygiene practice, fought
out on a state-by-state basis. Since the first law
in Colorado permitting independent practice,
California (1998) and New Mexico (1999) also
have enacted laws that permit dental hygienists
to own dental hygiene practices under some cir-
cumstances. Even more common is allowing
dental hygienists to practice without direct
supervision in public health settings, schools,
health centers, nursing homes, and similar
types of facilities. As of early 2004, 15 states had
provision for allowing some forms of unsuper-
vised practice in these types of facilities.33 As of
2003, state Medicaid regulations in 10 states
allowed dental hygienists to be paid directly for
dental hygiene services provided by them.34
Promoting expansion of dental hygienists’
autonomy continues to be a major activity of
the American Dental Hygienists’ Association. At
the same time, the ADA continues to watch and
often resist these moves.
Dental Assistants
Dental assistants are the most numerous of
all dental personnel groups in the United
States and, along with dental laboratory tech-
nicians, are the longest-established auxil-
iaries. They began to be employed with
regularity in dental practices toward the latter
part of the nineteenth century. The first assis-
tants were trained on the job by their dentist-
employers to aid in receiving patients and
performing “housekeeping” chores and office
clerical procedures. Many assistants today still
follow this same pattern, because formal
training and licensure are not required for
dental assistants who perform only the tradi-
tional extraoral functions .
In 2004 there were approximately 240,000
active dental assistants in the United States, or
about 150 per 100 active dentists.45 The ADA’s
1998 Survey of Dental Practice stated that 94.1%
of dentists in practice employed at least one
chairside assistant.29 The number of assistants
increased sharply during the 1970s and early
1980s, rising from an estimated 91 per 100
active dentists in 1965.96 Some of the increase
may be attributable to training programs in
dental schools, originally encouraged by federal
funds, in which dental students were taught
how to use assistants effectively. Another meas-
ure of increased utilization of assistants can be
seen in the same 1998 survey,29 in which more
than 60% of dentists reported employing two or
more assistants.
During the 1980s there was a decline in
training program enrollments that paralleled
those in dentistry and dental hygiene. The peak
first-year enrollment of 8386 in 1979 fell to
5388 in 1988,2 but then rose to 5669 in 1995.4
In 2004, approximately 250 institutions11
offered accredited training programs, about
double the number in 1968, although down
from the peak of 296 in 1980.
In most states, dental assistants are now
legally allowed to carry out more than their tra-
ditional duties. Many state laws and regulations
have been changed to allow expanded functions
of assistants. A bewildering and constantly
changing variety of tasks is permitted from one
state to another.27,41,53,64 In some states, no cer-
tification or licensure is required; in others,
certification is required; and in still others, test-
ing and registration are required. Voluntary
certification for dental assistants has been avail-
able since 1948 through the Certifying Board of
the American Dental Assistants Association,
now known as the Dental Assisting National
Board (DANB), and this certification is accepted
in some states as qualification to practice the
expanded functions defined in its dental prac-
tice act. About 30,000 dental assistants are
DANB certified.45
Expanded Function Dental Auxiliaries
Although dental assistants were used in the nine-
teenth century, it was not until the shortage of
civilian dentists during World War II, owing to
the enlistment of many dentists in the armed
services, that serious consideration was given to
their more efficient use.63 The introduction of
the air-turbine dental handpiece in the 1950s

removed much of the drudgery from cavity and
crown preparation and made greater productiv-
ity much more achievable. Development of
“four-handed dentistry,” with the dentist and
assistant both seated, was a natural consequence.
With it came sweeping changes in design of den-
tal chairs, operating equipment, access to instru-
ments, and layout of the dental office.
Continued developments in equipment,
materials, and procedures are constantly mak-
ing the role of the dental assistant more com-
plex. The chairside assistant in a busy office
must know instruments and understand proce-
dures well for this type of practice to work. In
the interest of greater operating efficiency, it was
inevitable, therefore, that assistants began to do
more and more intraoral procedures. Research
has shown that both hygienists and assistants
are capable of carrying out a wide range of extra
duties at a high level of quality when adequately
trained1,37,41,57,67–69,87 and that the productiv-
ity and income of dentists can be greatly
improved as a result.39,73,74,76,82
Moves toward utilization of EFDAs were
given impetus during the 1960s, when a critical
shortage of dental personnel was seen as immi-
nent. If the country were to be short of dentists,
the reasoning went, at least let those in practice
be as productive as possible. Federal funds
became available for dental schools to operate
Dental Auxiliary Utilization programs, which
trained dental students in four-handed den-
tistry, and later for Training in Expanded
Auxiliary Management programs, which taught
dental students to work with auxiliaries who
carried out an even wider range of functions,
including packing and carving amalgams in cav-
ities prepared by the students.
BOX 8-2 Examples of Duties Permitted To Be Carried Out by Expanded-Duty Dental Auxiliaries in the United
States27,35,78
●
Applying topical fluorides
●
Applying desensitizing agents
●
Applying pit-and-fissure sealants
●
Placing, carving, and polishing amalgam
restorations
●
Placing and finishing composite restorations
●
Placing and removing matrix bands
8 The Dental Workforce 121
The studies with EFDAs were carried out in a
variety of special institutional settings, although
considerable effort was made to simulate the
characteristics of the private office. Limited
studies in private offices also have been con-
ducted,47,73,74,79 and although they found
some difficulties in adjustment of office rou-
tines, they confirmed that EFDAs can be suc-
cessfully used there. EFDAs are also routinely
used in the Indian Health Service and military
and Department of Veterans Affairs facilities,
and by some private practitioners in states
where they are permitted.53,64,73,74 Examples of
the kinds of duties defined as expanded duties
in various state dental practice acts are shown in
Box 8-2.
The interest of government in promoting
EFDAs is in increased productivity and in the
subsequent presumed lower cost of care to the
public. In fact, the U.S. General Accounting
Office, in a 1980 report, urged states to develop
practice acts that permitted expanded functions
and recommended that all federal programs
make wider use of EFDAs.100
Although the research literature makes it
clear that auxiliaries can function as well as
dentists in providing these expanded services,
an appropriate cautionary note has been
sounded.41 A careful reading of the literature
shows that even though the candidates for the
demonstration projects were carefully selected
and received rigorous training, not all candi-
dates were able to perform successfully and
some were dropped from the programs. These
selective and rigorous training programs are
quite different from the requirements for
expanded functions in many states, some of
which require no formal training or evaluation
●
Placing and removing rubber dams
●
Monitoring nitrous oxide use
●
Taking impressions for study casts
●
Exposing and developing radiographs
●
Removing sutures
●
Removing and replacing ligature wires on
orthodontic appliances
122 Dental Practice
at all. Caution is needed because the evidence
that carefully trained auxiliaries can function at
high levels when adequately trained does not
necessarily mean that the same outcome can be
assured in the absence of such training.
The American Dental Association
and Expanded Function Dental Auxiliaries
A complicating factor in the legal status of
EFDAs in the United States has been the posi-
tion of the ADA, which, although it does not
directly or legally control state boards, clearly
has influence. During the mid-1960s, ADA pol-
icy encouraged experimental projects. By the
early 1970s, however, when many became con-
cerned about the possible oversupply of den-
tists, ADA policy reversed its stance and
opposed such experimentation. As one health
economist noted, an increase in EFDAs at the
same time as an increase in dentists would
clearly have a negative impact on dentists’ will-
ingness to employ them.50
Because most of the research studies on the
use of EFDAs were based in dental schools,
some dental educators became irritated at what
they perceived as the ADA’s efforts to interfere
with academic freedom. The ADA’s mood con-
tinued to become more opposed to experi-
ments with EFDAs, however, and since 1975 the
House of Delegates has passed a series of resolu-
tions to that effect. These resolutions are
opposed to (1) delegation of many of the proce-
dures now permitted in some states, such as the
taking of final impressions, placement or
adjustment of appliances, performance of intra-
oral restorative procedures, and the use of local
anesthetics; and (2) independent or unsuper-
vised practice of any auxiliary personnel.16,18,20
Despite all of these activities with expanded
functions over the last three decades, suggestions
to develop operating auxiliaries like the New
Zealand dental therapist (see Chapter 6) are rare.
Part of the reason may be that, in the late 1940s,
an attempt was made to establish such a plan in
Massachusetts, but it was stopped by swift and
effective political action by organized den-
tistry.48 The recent initiation of a limited dental
therapist program in Alaskan native communi-
ties (see Chapter 6) is a notable exception.
A possible additional reason for reduced
enthusiasm about EFDAs is the change in the
types and level of restorative need that has
accompanied the decline in dental caries. The
greatest benefits in increased productivity with
EFDAs come with routine restorative care.
Several decades ago it was quite common for
children to require multiple restorations at each
dental visit, and with the use of EFDAs, the
process of quadrant and half-mouth restorative
care was common. Today, however, the number
of restorations placed per patient has declined
substantially,28,49 and therefore the poten-
tial efficiency of using EFDAs may also have
declined.
Dental Laboratory Technicians
The dental laboratory technician, like the dental
assistant, has been a part of dentistry for a long
time. The technician’s task is to fabricate crowns,
bridges, dentures, and orthodontic and other
appliances on the prescription of a dentist.
Many of these tasks require high precision, and
the technician’s skill weighs heavily on the ulti-
mate success of the treatment. Although many
laboratory technicians are trained on the job,
there are approximately 30 dental technology
programs in the United States accredited by the
ADA’s Commission on Dental Accreditation.13
Technicians also may become certified dental
technicians in one or more of the areas of com-
plete dentures, partial dentures, crowns and
bridges, ceramics, and orthodontics.
Traditionally technicians were directly
employed by dentists and worked in a labora-
tory in the same office as the dentist. Over time,
however, this arrangement became uneconomi-
cal for most dentists. In addition, some techni-
cians have become specialists, whose skills are
properly at the disposal of many dentists. Most
technicians now are employed by independent
commercial laboratories, which provide their
services to dentists. In the ADA’s 1998 Survey of
Dental Practice, only 6.8% of responding den-
tists directly employed a laboratory technician
either full or part time.29
The ADA estimated that in 1997 there were
about 60,000 active technicians in the United
States, or 40 per 100 active dentists. Enrollment
in accredited training programs has declined
from a peak of 1665 first-year enrollees in 1981
to 908 in 1990 and 487 in 1998.2,24,61 These
continuing declines in enrollments are causing
some concern that it will become increasingly
difficult for many dentists to find competent

laboratory services.15,86,104 Factors that affect
the national staffing picture are relatively
low hourly wages in the industry, growth in
the use of dental laboratories overseas in low-
wage countries, and a general decline in the
need for some types of laboratory services
because of changing patterns of disease in the
population.
Denturists
During the 1970s and early 1980s, some dental
laboratory technicians tried to change state den-
tal practice acts to allow them to treat the public
directly for the fabrication of dentures. These
technicians call themselves denturists and their
occupation denturism. This activity came at
approximately the same time as similar move-
ments in Canada. Denturists are now legally
recognized in most Canadian provinces and
six states (Arizona, Idaho, Maine, Montana,
Oregon, and Washington). The requirements
for licensing vary among the states but usually
include some educational component.
The ADA has vigorously opposed the dentur-
ist movement. Its principal argument is that
denturists are unqualified to treat patients and
that poor-quality care and even actual harm
could result to patients. In 1973 the ADA
defined denturism as “the fitting and dispens-
ing of dentures illegally to the public,”17 a defi-
nition both clear and brief, even if no longer
accurate for some states. Although the sound-
ness of the ADA’s argument may be evident in
dental circles, it may be less so to the public and
to legislators. This fact became painfully clear in
the 1978 Oregon elections. Supporters of den-
turism had put the subject on the election ballot
through the statewide initiative process, which
meant that if it succeeded, the measure auto-
matically became law. Not only was it success-
ful, but the 3:1 margin of victory stunned
organized dentistry. The conclusions of the
ADA’s postmortem analysis were as follows:
●
The public viewed denturism as a con-
sumer issue, not a health issue.
●
The public believed that dentistry’s
campaign was spurred by economic self-
interest.
●
Some votes were based on sympathy for the
elderly.
●
Denturism provided consumers with free-
dom of choice.
8 The Dental Workforce 123
●
The media campaign organized by den-
tistry through a public relations firm
was widely perceived as tasteless and
unprofessional.7
The issue seems to have settled down from its
peak in 1980, perhaps because in those states
where denturists practice legally there appears
to have been no major rush by patients to seek
their care. With declining edentulism in the
United States (see Chapter 19), the importance
of the issue should continue to fade.
LEGISLATIVE INFLUENCE ON
DENTIST SUPPLY AND DISTRIBUTION
Federal programs to provide financial aid to
training institutions and to students between
1963 and 1980 were first intended to increase
the supply of certain types of graduates. Legisla-
tion in the 1970s then attempted to alleviate the
maldistribution of health personnel. However,
what should be done about maldistribution
continues to be a subject of debate. Some
believe that a sufficient supply of dentists will
permit free-market forces to sort out any prob-
lems. Some redistribution through the free
movement of dentists undoubtedly does occur,
but it also takes time and may be only partially
effective. Others believe that only significant
changes in the dental care system will solve the
problem. If dentists are left as free as they now
are to choose a practice location, so this argu-
ment goes, maldistribution will continue.
National Health Service Corps
One federally sponsored program aimed
directly at easing maldistribution of health care
providers is the National Health Service Corps
(NHSC), the result of 1971 legislation.80 The
NHSC is designed mainly for physicians, but
dentists and dental hygienists are also eligible.
Although initially based on volunteers, the pro-
gram has at various times provided scholarships
and loan forgiveness to recent graduates to
encourage them to practice in designated short-
age areas.
After reaching a peak in 1980, when 6409
scholarships were awarded (both medical and
dental), the program came under considerable
strain. Severe budget cuts were enacted during
the 1980s; by 1989 the scholarship program
had ceased. Throughout the same period, a
124 Dental Practice
growing problem developed with defaults on
student loans. The usual requirement was that
each year of educational tuition and living
expense support would be repaid by 1 year of
practice in a shortage area, but by 1987 more
than 1300 scholarship recipients were in default
by having refused to serve in shortage areas.43
The phasing out of the scholarship program
led to a rapid decline in the number of den-
tists going to shortage areas, which itself
suggests that the scholarship program was
achieving its goals. Community health centers
(see Chapter 6) were particularly hard hit,
because a high percentage of their staff had
come from the scholarship programs. The pro-
gram continues mainly through a loan repay-
ment system, and as of 2004, a qualifying
practitioner practicing in a federally designated
health professional shortage area was poten-
tially eligible for loan repayment of up to
$25,000 per year for the first 2 years of service.92
Subsidies to Dental Schools and Dental
Students
Before and since the NHSC, governmental pro-
grams to increase the supply of dental person-
nel existed in the form of financial incentives to
dental schools and subsidies to dental students.
Most dental schools are constructed and largely
supported by state governments. Their object is
to supply dentists for the state concerned, as
indicated by the standard practice of charging
higher rates of tuition for out-of-state residents.
Although some federal money has gone into
dental schools for decades, the proportion of
dental school budgets that come from federal
funds rose dramatically in the years up to the early
1970s. The Health Professions Educational Assis-
tance Act of 1963 was designed to alleviate the
perceived shortage of health personnel, including
dentists. This legislation subsidized existing
schools, provided funds for new construction and
renovation, and provided direct aid to students,
all with few strings attached. An intended effect of
this legislation was the sharp increase in the num-
ber of dental graduates (see Fig. 8-1).
The Comprehensive Health Manpower Act of
1971 continued financial aid to schools but
with some stricter provisions for the use of the
money attached. This act was followed by a
period of financial recession, inflation, slower
population growth, and growing belief in some
dental circles that the perceived shortage of den-
tists had been alleviated and was tending
toward an oversupply. The Health Professions
Educational Assistance Act of 1976 was thus
enacted in a different atmosphere from that of
1963. It concentrated on improving the distri-
bution of primary care personnel rather than on
simply increasing numbers. Part of the act’s
requirements were that dental schools could
qualify for federal support funds only if they
either (1) increased enrollment of first-year stu-
dents by a specified proportion, or (2) provided
“off-site” training for dental students. Some
dental schools declined the federal aid rather
than accept these conditions.
Between the mid-1970s and mid-1980s,
there were substantial reductions in federal sup-
port to dental education. The institutional
support grants that dental schools had come to
rely on were eliminated. As a source of school
operating revenue, federal funding fell from
nearly 30% in 1973 to just over 10% by the early
1980s, where it has remained. The result has
been intense financial pressure, reflected in
higher tuition costs, because few states were
able to fill the financial gap left by the loss of
federal funds. To make matters more difficult,
the reduced number of applicants put limits on
how high tuition could go and therefore how
much of the budget it could cover.
It is worth remembering that student tuition,
high as it is and with an average indebtedness of
$118,750 per graduate in 2003,31 represents
well under half of the cost of a dental student’s
education. At public dental schools in 1998,
only about 15% of revenue came from tuition;
in private schools it was just about 53%.15 The
combination of these pressures led to the deci-
sion during the late 1980s and early 1990s by
six dental schools (all private) to close. Since
1997, however, three new dental schools (Nova
Southeastern University College of Dental
Medicine; University of Nevada, Las Vegas,
School of Dental Medicine; and Arizona School
of Dentistry and Oral Health) have opened, the
first new dental schools in several decades.
There may be more changes as dental education
struggles to adjust to the new realities of
extremely high costs of dental education, popu-
lation shifts, generally stagnant levels of govern-
mental support, and potential pressure on
academic health centers, brought on by the

demands of managed care, to reduce costs.38
These negative forces may be balanced, how-
ever, by the generally favorable economic pic-
ture for dentists at the turn of the twenty-first
century36,42,72,105 and the apparent increase in
the number of applicants to dental schools.
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Assoc 1971;82:1067–81.
70. Mann WR. Dental education. In: Hollinshead BS: The
survey of dentistry: The final report. Washington DC:
American Council on Education, 1961:239–422.
71. Martens L, Glasrud PH, Burton KL. A profile of
Minnesota’s younger women dentists [abstract]. J Dent
Res 1985;64:205.
72. Meskin LH. Healthier, wealthier and wiser. J Am Dent
Assoc 1998;129:1660, 1662.
73. Milgrom P, Bergner M, Chapko MK, et al. The
Washington state dental auxiliary project: Delegating
expanded functions in general practice. J Am Dent
Assoc 1983;107:776–80.
74. Mullins MR, Kaplan AL, Bader JD, et al. Summary
results of the Kentucky dental practice demonstration:
A cooperative project with practicing general dentists.
J Am Dent Assoc 1983;106:817–25.
75. Niessen LC, Kleinman DV, Wilson AA. Practice char-
acteristics of women dentists. J Am Dent Assoc
1986;113:883–8.
76. Pelton WJ, Overstreet GA, Embry OH, Dilworth JB.
Economic implications of adding one therapist to a
practice. J Am Dent Assoc 1973;86:1301–9.
77. Perry DA, Freed JR, Kushman JE. The California demon-
stration project in independent practice. J Dent Hyg
1994;68:137–42.

78. Pontecorvo DA. Expanded duties: Results of ADAA’s
nationwide survey. Dent Assist 1988;57(4):9–13.
79. Redig D, Snyder M, Nevitt G, Tocchini J. Expanded duty
dental auxiliaries in four private dental offices:
The first year’s experience. J Am Dent Assoc
1974;88:969–84.
80. Redman E. The dance of legislation. New York: Simon
and Schuster, 1973.
81. Reveal M. Dental hygiene regulation and practice. J
Public Health Dent 1989;49:228–30.
82. Romcke RG, Lewis DW. Use of expanded function
hygienists in the Prince Edward Island manpower
study. J Can Dent Assoc 1973;39:247–62.
83. Santangelo MV. A review of dental school accreditation:
Development and current philosophy. J Dent Educ
1977;41:233–8.
84. Santangelo MV. The dental accrediting process. J Dent
Educ 1981;45:513–21.
85. Selden WK. Study of accreditation of selected health
educational programs. Part one: Working papers.
Washington DC: National Commission on Accrediting,
1971.
86. Shortage of qualified dental technicians. Gen Dent
1993;41:288, 290.
87. Soricelli DA. Implementation of the delivery of dental
services by auxiliaries: The Philadelphia experience. Am
J Public Health 1972;62:1077–87.
88. Talbot NS. Why not more women dentists? J Dent Educ
1960;60:114–22.
89. Tillman RS. Women in dentistry—a review of the litera-
ture. J Am Dent Assoc 1975;91:1214–20.
90. Tillman RS, Horowitz SL. Practice patterns of recent
female dental graduates. J Am Dent Assoc 1983; 107:32–5.
91. US Department of Commerce, Bureau of the Census.
Historical statistics of the United States: Colonial time
to 1957. Washington DC: Government Printing Office,
1960.
92. US Department of Health and Human Services, Health
Resources and Services Administration, Bureau of
Health Professions. Fiscal year 2004 loan repayment
program applicant information bulletin. E. Benefits.
93. US Department of Health and Human Services,
Health Resources and Services Administration,
Bureau of Health Professions. US health workforce
personnel factbook, website: http://bhpr.hrsa.gov/
healthworkforce/reports/factbook02/FB301.htm.
Accessed February 16, 2004.
94. US Department of Health and Human Services, Public
Health Service, Health Resources and Services
Administration. Factbook—health personnel United
States. Washington DC: Government Printing Office,
1993.
95. US Department of Health and Human Services, Public
Health Service, Health Resources and Services
8 The Dental Workforce 127
Administration. Factbook—health personnel United
States. Washington DC: Government Printing Office,
1997.
96. US Department of Health and Human Services, Public
Health Service, Health Resources and Services
Administration. Sixth report to the President and
Congress on the status of health personnel in the
United States. DHHS Publication No. HRS-P-OD-88-
1. Washington DC: Government Printing Office,
1988.
97. US Department of Health, Education and Welfare,
Public Health Service, Bureau of Health Manpower.
Dental manpower fact book. DHEW Publication No.
(HRA) 79-14. Washington DC: Government Printing
Office, 1979.
98. US Department of Health, Education and Welfare,
Public Health Service, Division of Dental Health.
Manpower supply and educational statistics for den-
tists and dental auxiliaries. Bethesda MD: Division of
Dental Health, 1972.
99. US Department of Labor, Bureau of Labor Statistics.
Occupational outlook handbook 2004-05 edition.
Bulletin 2540. Dental hygienists, website: http://
www.bls.gov/oco/print/ocos097.htm. Accessed May
12, 2004.
100. US General Accounting Office. Increased use of
expanded function dental auxiliaries would benefit
consumers, dentists, and taxpayers. Publication No.
HRD-80-51. Washington DC: Government Printing
Office, 1980.
101. Vernon TM. The licensure of dental hygienists in
Colorado: An update. J Public Health Dent 1989;
49:234.
102. Waldman HB. Female dentists: A factor in determin-
ing the available future dental work force. J Am Coll
Dent 1985;52(4):22–7.
103. Waldman HB. Pediatric dentists: Evolving demo-
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104. Waldman HB. Will there be enough trained dental
auxiliaries? Ill Dent J 1992;61:253–6.
105. Weeks WB, Wallace AE, Wallace MM, Welch HG.
A comparison of the educational costs and incomes of
physicians and other professionals. N Engl J Med
1994;330:1280–6.
106. World Health Organization. Report of an expert com-
mittee on auxiliary dental personnel. Technical Report
Series No. 163. Geneva: WHO, 1959.
107. World Health Organization. Inter-regional seminar
on the training and utilization of dental personnel
in developing countries, New Delhi, India, Dec
1967. WHO Document DH/68.2. Geneva: WHO,
1968.
108. Zillen PA, Mindak M. World dental demographics. Int
Dent J 2000;50:194–7.
 9 Access to Dental Care
REASONS FOR ACCESS PROBLEMS
SCOPE OF THE ACCESS PROBLEM
SUPPLY OF DENTISTS
Adequacy of the Supply of Dentists
Factors Determining Adequacy
Access Problems for Certain Populations
STRATEGIES TO SOLVE THE ACCESS PROBLEM
Strengthening of the Safety Net System
In 2001, 65.6% of people ages 2 years and older
in the United States reported that they had
visited a dentist within the previous year.30
According to a survey of American adults in
2003, slightly over 82% reported having a regu-
lar dentist.7 These figures show that, for a large
portion of the U.S. population, access to dental
care is more routine than ever. But for a dis-
turbingly large subset of the population regular
access is not so simple. It is perhaps easy for
many dentists in busy practices not to fully
appreciate the difficulty experienced by many of
those who do not get regular care, because their
attention, understandably, is directed toward
providing care to their established patients.
Among those with lower levels of access are the
poor, members of minority groups, the elderly,
the very young, the institutionalized, and those
with many types of disabilities. People living in
sparsely populated rural areas or in run-down
urban areas, where dentists are few, also have
much reduced access to care. Often several of
these characteristics apply simultaneously,
which makes the situation especially difficult.
Access is a complex, multidimensional concept.
It is also a continuum, not a matter of presence or
absence. How much access is the right amount is
probably undefinable in absolute terms, at least
partly because how much is enough differs from
one person to another and even for the same per-
son over time. Defining adequate access also is
128
Provision of Adequate Payment
Optimal Use of Allied Dental Personnel
Special Arrangements for Special
Populations
Development of Cultural Competency
Expansion of the Mindset of Dentistry
Establishment of Responsibility for Providing
Needed Resources
complex because the ability to overcome impedi-
ments to access varies from person to person.
REASONS FOR ACCESS PROBLEMS
There are a multitude of reasons for access prob-
lems, and many of them are caused or made
worse by lack of resources. Often this lack of
resources is as simple as not having money to pay
the usual fees for dental care. In other cases, it can
be lack of program funds needed to meet the
costs of providing care for the homebound, the
very young, and people with disabilities. In still
others, it can be lack of resources to ensure that
health care personnel have developed compe-
tence beyond the norm required to deal with
some of these special needs. Providing the means
to overcome physical barriers also can be expen-
sive, and cultural mismatches between providers
and patients from ethnic minorities also can pres-
ent a substantial barrier. People who are not in
the mainstream of the population due to minor-
ity or immigrant status, inadequate financial
resources, compromised mobility, or special
needs simply do not have the ready access to den-
tal care that is enjoyed by most of the population.
SCOPE OF THE ACCESS PROBLEM
The number of people enrolled in Medicaid
in 2002 in the United States was estimated at

39.9 million, of whom 18.4 million were chil-
dren.26 By definition, all of these individuals
need financial help to pay for dental care.
Medicaid coverage for dental care is mandated
for children (although it is chronically under-
funded, see Chapter 7), but for adults any
Medicaid dental care beyond the most rudi-
mentary emergency services is now rare. In 2002
there were another 4.2 million children enrolled
in the State Children’s Health Insurance
Program (see Chapter 7). In addition, of the
40.6 million individuals enrolled in Medicare
in 2001, over 5.5 million were disabled (and
under age 65) and approximately 4.5 million
were 85 years or older, people who were likely
to have mobility problems in accessing conven-
tional dental practice. There is virtually no den-
tal coverage in Medicare. These groups contain
many of the people most likely to experience
access problems, and they total nearly 50 mil-
lion individuals (Medicaid, plus the disabled
and those age 85 and older on Medicare), or
more than 300 people per dentist, on average.
Ensuring their dental care means that adequate
means of financing must be forthcoming.
Private dental practices, although they can and
do provide some care of this type on a pro bono
basis, require external help to provide care for
this many individuals.
The largely government-subsidized safety net
system, of which the migrant and community
health centers are the major part, does play
60
Dentists per 100,000 population
50
40
30
20
10
0
1970
Fig. 9-1 Number of dentists in the U.S. population per 100,000 people, actual and projected, for selected years,
1967-2020.3
9 Access to Dental Care 129
an important part in providing access where
it might otherwise not be unavailable. Never-
theless, there needs to be more of these facilities
and they need long-term support to be sustain-
able. In 2002 these health centers were able to
provide dental care to 1.6 million people,27
only a fraction of the nearly 45 million
Medicaid and State Children’s Health Insurance
Program enrollees. It is evident that both the
safety net system and private practices are
required if the needs of these populations are to
be met.
SUPPLY OF DENTISTS
It is tempting to blame lack of access on an
insufficient number of dentists, but this is
far too oversimplified. Of course, a sufficient
supply of dental personnel is necessary for
good access to dental care. The traditional way
to estimate the adequacy of the supply of
dentists has been the dentist/population ratio.
Fig. 9-1 shows the historical pattern in the
ratio of dentists to population in the United
States, with projections through the year 2020.
From a peak in the late 1990s, the supply of
dentists is projected to decline because of
(1) the growth in the U.S. population (see
Chapter 2), and (2) the impending retirement
of the large number of dentists who graduated
in the 1970s and 1980s, combined with smaller
dental school class sizes since then (see
1980 1990 2000 2010 2020 2030
Year
130 Dental Practice
Chapter 8). Even if dental school classes were
to be expanded to the peak seen in the late
1970s, it would take at least until the 2020s to
restore the dentist/population ratios of the
early 1990s.
In addition to measures of the dentist/popu-
lation ratio, the two other most commonly used
approaches to estimating personnel needs
are demand-based and need-based models. The
demand-based approach comes from economic
theory and aims to make forecasts of the quan-
tity of dental care that people will actually con-
sume. The price and supply of services are key
components of these models. Demand-based
models have been used by the Health Resources
and Services Administration of the U.S. Depart-
ment of Health and Human Services and by the
American Dental Association (ADA) for their
workforce forecasts.20,28,29 Through such mod-
els, it is possible to estimate how issues such as
changes in insurance coverage, income levels,
number of dentists, and population growth are
likely to affect the use of dental care.
Need-based approaches to personnel require-
ments come from a philosophically different
direction. Need-based models start from meas-
urements of treatment need in a population,
from which estimates are then derived of how
much treatment would be required to meet those
needs. The time required for treatment is added
across the entire population, and from that an
estimate of the number of required provider-
hours of care can be determined.31 A complica-
tion with the need-based approach is that both
the accumulated backlog of need and estimates
of future disease must be included. Other inher-
ent difficulties are that dentists can treat the same
condition in different ways and that demand is
often poorly related to need. Demand for some
types of care, cosmetic restorations, for example,
is difficult to predict, which complicates the
need-based approach even further.
Adequacy of the Supply of Dentists
Although the number of dentists relative to
population clearly is an important considera-
tion in estimating the adequacy of the supply
of dental care, by itself it is not a sufficient indi-
cation of shortage or surplus. Careful examina-
tion of Fig. 9-1 demonstrates this fact. In the
early 1980s, when there were about 50 dentists
per 100,000 population, there was widely con-
sidered to be “too many” dentists. Both the den-
tal press and the popular media of the early
1980s contain a number of articles about the
economic pinch that dentists were feeling
because of what was perceived as a shortage of
patients. Many dentists complained that they
were not as busy as they wanted to be. By way of
contrast, in the late 1990s, when there were
nearly 55 dentists per 100,000 population (rela-
tively about 10% more dentists), dentists
reported being busier than ever, and their
incomes had never been higher.8,19 The fact that
2000 persons per dentist was “not enough” in
1982 whereas 1800 people per dentist was
“plenty” in 2000 shows that additional factors
must be important in determining the adequacy
of the dentist supply.
Uncertainty over the supply of dentists is not
new. The meaning of the relative increase in the
number of dentists between 1970 and the mid-
1990s, followed by the projected decline over
the next several decades, has aroused consider-
able discussion.6,14,16,17,21,23,29 For many years
after World War II, both the dental profession
and the public accepted that a shortage of den-
tal personnel was imminent. It was expected
that significant increases in demand, stemming
from rising affluence, rapid increases in popula-
tion (the postwar baby boom; see Chapter 2),
and the high levels of caries at the time (see
Chapter 20), would overwhelm the ability of
the dental profession to provide all the care
needed. The influential 1961 report The Survey
of Dentistry18 recommended marked increases
in the number of dental graduates and auxil-
iaries and made projections of future personnel
shortages. Indeed, the population figures from
the 1960 U.S. census (Fig. 9-2) showed a con-
tinuing increase in the young population that, if
continued, was expected to severely tax many of
the nation’s resources.
In 1963 the ADA referred to “the impending
shortage of health personnel” as “probably the
most critical problem in the health field today”5
and again foresaw shortages in 1965.1 These
views were still in evidence in 1971, when the
ADA’s Task Force on National Health Programs
stated the following as a basic assumption:
The United States faces a shortage of dental personnel in the
next 20 years and the shortage will occur whether or not there
is a national dental health program.4
 9 Access to Dental Care 131

25

20
Population in millions

15

10

0+
4

9
4

9
-3

-3

-4

-4

-5

-5

-6

-6

-7

-7

-8

-8

-9

-9
0-

5-

-1

-1

-2

-2

10
30

35

40

45

50

55

60

65

70

75

80

85

90

95
10

15

20

25

Age
Fig. 9-2 Population of the United States by 5-year age increments, 1960.24

However, by the mid-1970s many in den- graduates fell as low as 3778 in 1993, substan-
tistry no longer accepted the existence of a per- tially lower than any of these projections, and
sonnel shortage.9,17 The combined effect of a based on first-year enrollments, we can say that
large increase in the numbers of graduates (see the number of dental graduates through the
Chapter 8), chiefly as a result of increased fed- early twenty-first century will not be much
eral support of dental schools, plus the large more than 4500 per year. This whole matter is a
and unforeseen drop in the rate of population further lesson that, although predictions are a
growth (Fig. 9-3), led to the increase in the rela- necessary basis for rational policy decisions,
tive supply of dentists. The ADA agreed in 1973 predicting the future remains a hazardous busi-
that the relative supply of dentists was going to ness indeed.
increase considerably by 1985,2 a notable rever- It now seems likely that the dentist/popula-
sal from its position of only 8 years before.1 tion ratio will slowly decline for the foreseeable
No one in the early 1960s could foresee the future, although the consequence of this trend
dramatic drop in fertility rates with the conse- on the practice of dentistry or the oral health of
quent lowering of the rate of population the public remains uncertain. It has become
increase, nor was the large decline in caries (see clear that there is no “correct” ratio of dentists to
Chapter 20) anticipated. A further projection in population; what may have been the “right”
1977 indicated that the supply of dentists number of dentists in one decade is not neces-
would slightly exceed demand by 1990.25 sarily “right” in the next. Although low levels of
Assumptions in this projection were that popu- caries are already reducing the need for treat-
lation growth would continue at the 1977 rate, ment in younger Americans,13 substantial need
that 43%-50% of the population would be cov- will remain for maintenance and repair of the
ered by dental insurance, and that the number restorations placed in earlier generations.6,10,22
of dental graduates would peak at 5460 in 1982 This trend may be magnified by increasing
and then remain stable through at least 1990. tooth retention (see Chapter 19). More adults
Of course, we now know that the number of will have relatively complete dentitions that
132 Dental Practice

25

20
Population in millions

15

10

0+
4

9
4

9
-3

-3

-4

-4

-5

-5

-6

-6

-7

-7

-8

-8

-9

-9
0-

5-

-1

-1

-2

-2

10
30

35

40

45

50

55

60

65

70

75

80

85

90

95
10

15

20

25

Age
Fig. 9-3 Population of the United States by 5-year age increments, 1980.24

they expect to maintain throughout life and will although market forces work well to regulate
thus require restorative and periodontal care. many aspects of the economy, health care pres-
Although it now seems likely that the adult ents a special challenge. Market forces attract or
population will have substantially reduced deter dental students based on conditions as
need for care a few decades from now, the les- they are now, and conditions can be very differ-
sons from the recent past should be ample ent in 20 years’ time. In its comprehensive report
warning that speculations about the future on the future of dental education, the Institute
should be treated as tentative at best. Even so, of Medicine gave the issue of the dental work-
getting the personnel numbers “right” for the force careful consideration.15 In the face of the
future demands policy now. The effects of many uncertainties already cited, the Institute of
policies like those embodied in the Health Medicine recommended keeping the first-year
Professions Educational Assistance Act of 1963 enrollment levels at about 4000 for the foresee-
are not seen for at least 10 years. Schools have to able future, a level that has already been passed
be built or expanded, faculty established, and by about 10% (see Chapter 8).
the first new classes moved through to gradua- Boxes 9-1 to 9-3 describe factors that are
tion and practice. Fig. 8-1 showed that the 1963 likely to play a role in determining the adequacy
act first began to have real impact on the num- of the supply of dentists and dental care. As we
ber of practicing dentists in the years 1970-75, have already seen, how these factors will bal-
and the effect of these graduates will be with us ance out is exceedingly difficult to predict.
at least through 2020. Nevertheless, at least in terms of traditional dis-
ease-based dental care, it seems reasonable to
Factors Determining Adequacy expect that, with the ever-accumulating effect in
Skeptical about what they see as governmental the population of the declines in dental caries
ineptitude, many leaders in dentistry (and some and related improvements in oral health, the
in government) would prefer to leave the matter average dental practice should in the future
of workforce numbers to market forces. But be able to manage the oral health of many

BOX 9-1 Factors Tending Toward a Shortage of Dentists
●
Good economic times. As people have more
disposable income, they are able to buy more dental
care. Some dental care can be postponed, and with
good economic times treatment for this postponed
care may then be sought.
●
High expectations for oral health. With the general
improvement in oral health that has occurred over the
past several decades, many people fully expect to
maintain a healthy dentition throughout life and are
willing to invest in dental care to that end.
●
Less edentulism. As tooth loss diminishes in the
population, there are more teeth to maintain
throughout life.
●
Growing utilization. Over the past several decades, a
growing proportion of the population reports
BOX 9-2 Factors Tending Toward a Surplus of Dentists
●
Falling disease levels. Treatment of disease has
historically been a major part of what motivates
patients to visit dentists, and treatment of the
consequences has been a major part of what dentists
do. As succeeding birth cohorts benefit from lower
disease levels, there will be less per patient for
dentists to treat.
●
Changes in utilization. As increasing numbers of
individuals who experienced low levels of dental
caries as children become young adults, they may not
need nor seek dental care as frequently as their
parents’ generation did.
●
Effects of the “baby bust” generation. In addition to
having lower levels of past disease than their parents’
generation, the birth cohorts since the early 1960 are
much smaller than the generation that came before
more patients than in the past.11 It is also the
case that, because of improving oral health, the
mix of dental services in most dental practices is
shifting toward those that can be provided by
allied dental personnel.13 These facts alone
should call into question concerns that a slowly
declining dentist/population ratio over the next
several decades is a sign of a looming shortage
of dentists.
It also is evident, in some cases at least, that a
shortage of dentists per se is not the problem in
9 Access to Dental Care 133
●
receiving dental care on a regular basis. As this
proportion continues to rise, more dental care will be
consumed.
●
Effects of the baby boom group in the population.
The bulge in the population that resulted from the
post–World War II baby boom (see Chapter 2) has
affected many aspects of life in the United States and
will continue to do so for several more decades.
Because these birth cohorts were children when
caries levels were high, they carried into adulthood
many heavily restored teeth that continue to require
increasingly expensive maintenance.
●
Decline in the dentist/population ratio. All else being
equal, fewer dentists means that less dental care will
be available.
them. Because middle-aged adults have traditionally
been the group that provided large amounts of income
to dental practices, the combination of much less need
per capita and millions fewer of such patients could
mean significantly less income to dental practices.
●
Economic downturns. Just as improving economic
conditions are associated with more demand for
dental care, the inevitable periodic economic
downturns will likely reduce demand for care,
especially for cosmetic services.
●
Increasing role of auxiliary personnel. With
improving oral health, a larger proportion of the
income to many dental practices comes from
procedures associated with periodic recall visits. As
more of these services are provided by auxiliary
personnel, the need for dentists will decline.
lack of access for Medicaid enrollees. In a
Medicaid demonstration program in Michigan,
when fee levels were linked to those paid for
privately insured patients and administration
was managed by a commercial carrier in the
same way as for private groups, access to care
improved virtually immediately. Before this
changeover, about 25% of dentists in the
involved counties had treated Medicaid patients
in the previous year. Within the first year of
the demonstration program, over 85% of the
134 Dental Practice
BOX 9-3 Factors Associated With Uncertainty Regarding the Adequacy of the Supply of Dentists
●
Possible changes in routine care. The patterns of
routine care, such as the 6-month recall visit, date to
times when disease levels in the population were
much higher than today and home care was less
effective. As the oral health of the population
continues to improve, the recommended time for
recall visits for the healthiest patients could be
significantly extended.
●
Demand for nondisease services. Future levels of
demand for services like cosmetic dentistry are
difficult to predict and are especially likely to be
subject to fluctuations associated with economic
trends.
●
Demand from healthy people. How the growing
proportion of the population who have experienced
little or no oral health problems will choose to use
dental care is uncertain.
●
Patterns of dentists’ retirements. The group of
dentists who graduated during the peak of dental
school enrollments will likely be retiring over the next
20 years or so. Because this group is so large, how
and when these dentists choose to retire will
dentists in the affected counties treated
Medicaid patients.12 Many more children
received dental care, and they received it with-
out having to travel excessive distances to find
an available provider. Although there clearly
had been a shortage in dental care available at
the conventional Medicaid fees, there appeared
to be no shortage when dentists were reim-
bursed at their usual fee levels.
Access Problems for Certain
Populations
Although there may be no across-the-board
shortage of dentists, and thus no access prob-
lems for most people, it bears repeating that
access will still be a problem for many. Those
most likely to experience access problems are
children, adults, and the elderly in families with
low incomes, people of all ages with disabilities
and special needs, and those living in areas
where there are few dentists (these most often
are low-income urban areas or low-population
rural areas). However, assuring adequate access
to dental care for these groups is not just a mat-
ter of training more dentists. Although dental
significantly affect the supply of dentists. However,
because dentists have so much flexibility in how they
practice, for example, in how many days per week
they practice and how many patients they see each
day, it is extremely difficult to predict these retirement
patterns.
●
Dental insurance trends. The major growth in dental
prepayment since the early 1970s has undoubtedly
had an important role in the recent high levels of
demand for dental care. However, that growth appears
to have plateaued, and if the pressures to reduce the
cost of health care (see Chapter 7) result in a
significant drop in the proportion of the population
with dental insurance, demand for dental care could
also drop.
●
Government role in dental care. Currently the role of
government in paying for dental care is small (see
Chapter 7). If dental coverage were to be added to
Medicare, or the coverage under Medicaid were to be
significantly improved, many people with high levels
of need could suddenly be brought into the dental care
system.
care for some of them, such as the disabled and
institutionalized, requires special training, the
major impediment to access is economic. It
takes money to operate a dental practice, and if
the patients don’t have the money to purchase
care, then access will continue to be a problem
unless supplemental sources of funding are
available. This will happen regardless of the
number of dentists trained. The primary condi-
tion for solving the problem of access to dental
care in the United States, in those places and for
those individuals for whom access is a problem,
is funding. Even the safety net providers of care
such as the community and migrant health cen-
ters (see Chapter 6) cannot provide access over
the long run without dependable long-term
funding.
STRATEGIES TO SOLVE THE ACCESS
PROBLEM
Because the reasons for access problems are
many and varied, solutions will also require a
multifaceted approach. The problem is too
large and too diverse to think that a single

approach will be adequate. Some of the
approaches that are likely to be essential to a
comprehensive solution are the following.
Strengthening of the Safety Net System
In many locations, both urban and rural,
economic or other conditions are simply not
adequate to support a sufficient number of con-
ventional dental practices. Local, state, and fed-
eral support is necessary to build clinics and in
many cases to subsidize the support of clinical
staff. The current system of community and
migrant health centers (see Chapter 6), which
are usually jointly supported by local, state,
and federal funds, is a prime example of this
safety net system. Without continuing public
support and additional support where new and
expanded clinics are needed, many locations
will remain areas of chronically low access.
Provision of Adequate Payment
For both the safety net providers and private
practitioners, reimbursement levels must be
adequate to cover the cost of providing care. It is
simply a fact that no system can continue to
exist in the long run if its costs are not met.
Although all providers willingly provide some
care without reimbursement, the size of the
population in the United States is too large for
such “free” care to be able to handle more than
a small fraction of the need.
Optimal Use of Allied Dental Personnel
Because of the generally improving oral health
of the U.S. population, a growing proportion of
the care that is provided could be managed by
auxiliary dental personnel. Dental practices
could thus become more efficient, with the abil-
ity to reduce the per capita costs of providing
dental care to many people. For this to happen,
some states will need to modify their dental
practice acts to permit practice by the types of
personnel most suited to providing the neces-
sary care under the most suitable practice
arrangements. Although the best solution will
vary from state to state, examples might include
liberalized licensing of foreign-educated den-
tists as proposed in California, independent or
unsupervised practice of dental hygienists,
expansion of functions for auxiliary personnel,
or use of dental therapists (see Chapters 6 and
8). If the cost of producing needed care can be
9 Access to Dental Care 135
reduced, it will be economically feasible to
provide care in places where otherwise it would
not be possible.
Special Arrangements for Special
Populations
In some circumstances, conventional dental
practices are simply not suited to providing ade-
quate access. For the elderly and disabled who
are confined to extended care facilities, care
often must be brought to them. Although some
practices are able to manage some of this kind
of care, many are not. Given the growing size of
the elderly population, it is likely that more
practices must be organized specifically for this
purpose for such care to be most efficient. As
with other forms of practice, sufficient treat-
ment funds must be forthcoming to make these
practices economically viable.
Development of Cultural Competency
Patient behaviors such as missing appoint-
ments and not following healthy lifestyles are
sometimes cited as reasons for the frustrations
that dental personnel experience in treating
some patients from low-income and minority
groups. Although it is appropriately a responsi-
bility of health care providers to attempt to
encourage optimum health-related behaviors, it
is also a responsibility to do so in a manner that
shows an understanding of the person’s capa-
bilities and circumstances. For example, for
many individuals and families in these unusual
circumstances, performing in ways that are typi-
cal of conventional patients can be exceedingly
difficult, and this must be taken into account in
working with them. The term cultural competency
is often used to denote the knowledge and skills
needed to be most effective in managing the
dental care of these individuals.
Expansion of the Mindset of Dentistry
For any of the aforementioned solutions to be
most effective they must have the strong sup-
port of the dental professions, both locally and
nationally. Although the primary focus of most
dental practitioners will necessarily be conven-
tional dental patients in conventional dental
practices, practitioners must also recognize that
nonconventional patients are as much a part of
their responsibility as are any other patients.
The discharge of that responsibility can take
136 Dental Practice
many forms, from welcoming all patients that
fit their practice arrangements to providing
encouragement and political support for those
practices that are organized to care for noncon-
ventional patients.
Establishment of Responsibility
for Providing Needed Resources
If the resources necessary to provide access are to
be in place, someone must be willing to provide
those resources. If that responsibility is not clearly
defined and those resources are not made avail-
able on an ongoing and dependable basis, access
will deteriorate. Discussions about improving
access that do not include the identification of the
resources to provide that access miss a necessary
component for long-term success.
Most of the people who suffer from inade-
quate access to dental care do so because they
simply do not have their own funds to pay for
dental care. Those funds will become available
only if society is willing to transfer funds from
people who have money to pay for the care of
those who do not. Until we as a society decide
to put sufficient funds into paying for this care
by adequately funding programs like Medicaid
so that dental practices can afford to provide
this care on a long-term basis, or by paying to
build and staff community clinics to serve
these populations, access is likely to remain a
problem.
The resource demands to meet even the most
modest definition of access in many groups
within the population are far beyond those that
dentistry alone can provide. The condition of
current federal and state budgets is driving
things in the wrong direction—with almost
every state dropping all but emergency services
for adults and looking for ways to further reduce
benefits for children. There also is a serious pro-
posal to reduce federal involvement in services
to the low-income population, as evidenced by
recent proposals to convert the federal Medicaid
matching funds to a block grant. This projected
move would include a cap on federal responsi-
bility in return for liberalizing the states’
requirements for comprehensive coverage of
children. The irony of this approach is that it
sets up a situation in which, just when people
most need this kind of help because of tempo-
rary difficult economic times, the state will be
least able to provide that help.
REFERENCES
1. American Dental Association, Bureau of Economic
Research and Statistics. Number of dental graduates
required annually to 1985. J Am Dent Assoc 1965;
71:697-8.
2. American Dental Association, Bureau of Economic
Research and Statistics. Growth in population and
numbers of dentists to 1985. J Am Dent Assoc 1973;
87:901-3.
3. American Dental Association, Health Policy Resources
Center. Future of dentistry. Chicago: ADA, 2001.
4. American Dental Association, Task Force on National
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Assoc 1971;83:569-600.
5. Association testifies in support of Educational
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Assoc 1989;119:117-21.
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scoop on your patients. ADA News 2004;35(8):1.
8. Brown LJ, Lazar V. Dentists and their practices. J Am
Dent Assoc 1998;129:1692-9.
9. Butts HC. Dental manpower shortage? [editorial]. J Am
Dent Assoc 1976;93:507.
10. Douglass CW, Furino A. Balancing dental service
requirements and supplies: Epidemiologic and demo-
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11. Eklund SA. Dentistry 2000—clinical care: Changing
treatment patterns. J Am Dent Assoc 1999;130:
1707-12.
12. Eklund SA, Pittman JL, Clark SJ. Michigan Medicaid’s
Healthy Kids Dental program. An assessment of the
first 12 months. J Am Dent Assoc 2003;134:1509-15.
13. Eklund SA, Pittman JL, Smith RC. Trends in dental care
among insured Americans: 1980 to 1995. J Am Dent
Assoc 1997;128:171-8.
14. Feldstein PJ. Financing dental care: An economic analy-
sis. Lexington MA: Heath, 1973.
15. Field MJ, ed. Dental education at the crossroads:
Challenges and change. Washington DC: National
Academy Press, 1995.
16. Furino A, Douglass CW. Balancing dental service
requirements and supplies: The economic evidence.
J Am Dent Assoc 1990;121:685-92.
17. Goodman SE. The dentist shortage that never was. Dent
Manage 1976;July:33-8.
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report. Washington DC: American Council on
Education, 1961.
19. Meskin LH. Healthier, wealthier and wiser. J Am Dent
Assoc 1998;129:1660, 1662.
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projections. J Dent Educ 1987;51:219-23.
21. Pew Health Professions Commission. Critical chal-
lenges: Revitalizing the health care professions for the
twenty-first century. San Francisco: UCSF Center for the
Health Professions, 1995.
22. Reinhardt JW, Douglass CW. The need for operative
dentistry services: Projecting the effects of changing dis-
ease patterns. Oper Dent 1989;14:114-20.

23. Solomon ES. Errors in federal report on dental health
personnel presents problems. J Dent Educ 1990;
54:499-501.
24. US Department of Commerce, Bureau of the Census.
1980 Census of the population. Vol 1, Characteristics of
the population, Chapter A, Number of inhabitants, Part
1, United States summary. Table 45. Washington DC:
Government Printing Office, 1983.
25. US Department of Health, Education and Welfare,
Public Health Service, Division of Dentistry.
Projections of national requirements for dentists
1980, 1985, and 1990. DHEW Publication No. (HRA)
77-48. Washington DC: Government Printing Office,
1977.
26. US Department of Health and Human Services, Center
for Medicare and Medicaid Services, Office of Research,
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Accessed May 13, 2004.
27. US Department of Health and Human Services, Health
Resources and Services Administration, Bureau of
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rollup), website: http://bphc.hrsa.gov/uds/data.htm.
Accessed May 6, 2004.
28. US Department of Health and Human Services, Public
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Administration. Health personnel in the United States.
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HRS-P-OD-92-1. Washington DC: Government
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Washington DC: Government Printing Office, 1990.
30. US Department of Health and Human Services, Public
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_US/hus03/Table078.xls. Accessed April 27, 2004.
31. World Health Organization. Health through oral
health. Guidelines for planning and monitoring for
oral health care. London: Quintessence, 1989.
 10 The Healthy Dental Practice: Infection
Control and Mercury Safety
INFECTION CONTROL
Guidelines for Infection Control
OSHA and Dental Practice
HIV INFECTION AND AIDS
Oral Manifestations of HIV Infection
HEPATITIS B AND C
PUBLIC AND PROFESSIONAL PERCEPTIONS
OF INFECTIOUS DISEASES
In dental practice not long ago, a blood-stained
swab after a tooth extraction was simply thrown
in the trash without further thought. Not any
more. Today, dental offices must use standard pre-
cautions, a set of procedures based on the assump-
tion that any patient, or any person working in
the dental office, might carry a serious infection.
All phases of dental treatment are then conducted
so as to minimize the risk of cross-infection.
Some dentists look with nostalgia on the old
days, a time when they did not have to work in
gloves, mask, and eyewear; ensure that office
waste went into the appropriate container; and
worry about the latest regulations from the U.S.
Occupational Safety and Health Administration
(OSHA). This nostalgic view is misplaced. It is
fair to say that dentistry should have been a lot
more concerned about cross-infection in the
old days than it was; it took a jolt from the
human immunodeficiency virus (HIV) epi-
demic to force improvement. Although some
dentists still see OSHA’s regulations on waste
disposal as just another bureaucratic burden,
the management of the office environment has
clearly become an integral part of running a
modern dental practice. Given that many more
people are infected with the HIV and hepatitis
B and C viruses than demonstrate overt disease,
the only defensible approach is to assume that
any patient could be infected and to act accord-
ingly. Dental practices today are far healthier
138
HIV ISSUES IN DENTAL PRACTICE AND
DENTAL EDUCATION
DENTAL UNIT WATERLINES
DENTAL AMALGAM: SAFETY AND
ENVIRONMENTAL ISSUES
environments than they ever were, and both the
public and the professions will continue to ben-
efit as a result.
Our purpose in this chapter is to review the
principal infection concerns in dental practice:
HIV, hepatitis B virus (HBV), and hepatitis C
virus (HCV). The chapter also reviews the issue
of mercury safety as an example of an environ-
mental concern.
INFECTION CONTROL
After the emergence of antibiotics during World
War II (1939-45), the industrialized world lost
much of its age-old concerns about infectious
diseases. The major epidemics of the past were
gone, and parents no longer feared the worst
when they heard a child cough in the night. It
was a short, complacent period during which
some of the painful antisepsis lessons from the
nineteenth century were neglected in our
dependence on antibiotics. This period ended
suddenly in the early 1980s with the harsh
reminder that mortal infectious diseases were
still with us. Not only is HIV infection a devas-
tating disease that shredded the social fabric
in a way not seen since tuberculosis in the
nineteenth century, but the HIV epidemic is
a humbling reminder that the path of biomed-
ical advancement is not always smoothly up-
ward.
 10 The Healthy Dental Practice: Infection Control and Mercury Safety 139
Of course, HIV infection is not the only infec-
tious disease to raise concerns about cross-
infection during dental treatment. HBV
infection is an ominous threat, and the risk of
HBV infection is higher in the unprotected den-
tal practice setting than in most other environ-
ments. Hepatitis B was around long before HIV
infection, but it took the impact of HIV infec-
tion to force adoption of those old-fashioned
barrier techniques of infection control that had
never been a routine part of dental practice.
Guidelines for Infection Control
The American Dental Association (ADA) had a
set of rather gentle infection-control guidelines
in the pre-HIV era,13 mostly concerned with hep-
atitis, but the advent of HIV in the early 1980s led
to a more stringent approach. Detailed guide-
lines were then developed by the ADA,16 and the
American Association of Public Health Dentistry
produced its guidelines in 1986.4 The definitive
guidelines for dental practice, however, are those
issued by the U.S. Public Health Service’s Centers
for Disease Control and Prevention (CDC).
These definitive guidelines were first issued in
1993,103 and the updated and considerably
extended version was released in late 2003 after
extensive public comments.104 The CDC has also
developed infection control guidelines for field
examinations for surveys or research studies.98
The ADA has now merged its statement on infec-
tion control with the CDC guidelines.
All of these guidelines are based on the con-
cept of standard precautions (previously called
universal precautions). The underlying philoso-
phy is that infected patients cannot be differenti-
ated from uninfected ones, so the prudent thing
to do is to assume that all patients may be
infected. A parallel approach, first presented in
1987,65 is referred to as body substance isolation,
which focuses on reducing transmission of
infectious material from any moist body sub-
stance of the patient to the health care worker.
Both approaches emphasize that barrier proce-
dures should be employed in treating all
patients, which means that gloves, masks, and
protective eyewear should be worn by dental
personnel. They also focus on proper disposal of
one-time-use materials, routine sterilization of
other instruments and equipment, and proper
handling of potentially infectious materials. The
2003 CDC guidelines moved toward combining
the previous universal precautions regarding
body substance isolation into a single set of
recommendations known as standard infection-
control procedures.70 Each recommendation in
these guidelines is graded according to the
strength of the scientific evidence to support it.
The barrier principles that form the basis of the
CDC guidelines hark back to the beginnings of
antiseptic medical practice, and they are effective:
HBV infection was found to be twice as high
among dentists who never wore gloves as among
dentists who wore gloves routinely.48 With stan-
dard precautions, the risk of transmission of either
HIV or HBV in the dental office is extremely low.29
OSHA and Dental Practice
OSHA was established by Congress as an agency
in the U.S. Department of Labor in December
1970 (Public Law 91-596), and some amend-
ments to the original act were passed in
November 1990. The mission of this regulatory
agency, as laid out in the introduction to the
original act, is “to assure safe and healthful
working conditions for working men and
women.” OSHA is responsible for establishing
standards for safe and healthy working condi-
tions for all employees and regulating mainte-
nance of these standards. OSHA’s standards
cover just about all industries: mining, ship-
ping, construction, logging, food service, health
care, and many others. OSHA also has standards
that are specific to workers handling hazardous
or potentially hazardous substances and mate-
rials, so the reach of this federal agency is
considerable. A number of states have set up
their own OSHA-type agencies, and OSHA is
required to work cooperatively with them.
Dentists, like all other employers, are subject
to occupational health and safety laws and
regulations that cover a variety of activities in the
dental office. Although OSHA’s interests include
a wide range of issues like ergonomics, water-
lines, and indoor air quality, the OSHA regula-
tion that has most affected dental practitioners
is the bloodborne pathogen (BP) standard. This
standard came into effect in March 1992 after a
period of intense public debate in which the
ADA played a prominent role. The BP standard
was revised in January 2001.102 It applies to all
activities in which health care workers come into
contact with human blood or other bodily flu-
ids, or are in a position where they may do so.
140 Dental Practice
The BP standard applies to hospitals and other
medical facilities, paramedical and ambulance
services, blood banks, research facilities, and of
course dental offices. The BP standard is com-
prehensive and highly detailed. It requires each
dental office to prepare an exposure control
plan, which is intended to minimize employee
exposure to infection. The BP standard covers
instrument sterilization and storage, handling of
potentially contaminated equipment, disposal
of medical waste, and many related topics.
It specifies that dentists must offer HBV vac-
cination to staff and includes meticulous
requirements for reporting “incidents,” that is,
accidents in which skin has been broken (e.g., a
needlestick) and hence in which there is poten-
tial risk of infection. Details get down to the
level of washing and storing laundry.
The ADA has not had a good relationship
with OSHA in the development and application
of these standards. The ADA has complained
that it was not consulted adequately prior to the
promulgation of the BP standard and that
OSHA indiscriminately and inappropriately
lumped dental practice in with hospitals and
other facilities. The ADA considered that OSHA
made no good attempt to understand dental
practice, and its calls for industry-specific stan-
dards were not heeded. OSHA inspects health
care facilities in response to complaints, and
soon after the BP regulations went into effect
the ADA began receiving complaints from den-
tists that some OSHA inspections of dental
practices were heavy-handed and clumsy. OSHA
admitted that there was some justification for
these complaints, and with better communica-
tions the relations between the two organiza-
tions improved somewhat. A major step in
improved relations came when OSHA permit-
ted dentists to respond to complaints by phone
or fax rather than be subjected to a site visit.
For dentists unaccustomed to reading the
language of the federal government, the BP
standard is a formidable document. To help
practitioners meet the standards, the ADA has a
set of manuals that outline the elements of an
exposure control plan and put infection-control
guidelines together with OSHA guidelines in
standard operating routines for the dental
office.5
Dentists have also complained about the high
cost of compliance with OSHA standards,32
sometimes implying that these are dollars not
well spent. Some of the more trivial aspects of the
BP standard have been refined over time, which
should have the effect of reducing costs, but com-
pliance will always carry some price. In the long
run it is patients who foot the bill, and so far the
public seems to view the cost of compliance as
money well spent.
HIV INFECTION AND AIDS
AIDS is the acronym for acquired immunodefi-
ciency syndrome and is the end point of HIV
infection. With the dominant position this con-
dition now occupies in the lives of all health
professionals, it is sobering to recall that HIV
was identified only in 1983.76 The knowledge
that has accumulated since then on the virology
and epidemiology of the condition represents
some impressive research, although the public
hysteria that can surround AIDS is a reminder
that humans have not fundamentally changed
much since the Black Death in the fourteenth
century.
The AIDS virus is human T-lymphotropic
virus type 3 or lymphadenopathy-associated
virus, a retrovirus usually called HIV. It attacks
the CD4+ T lymphocytes in infected humans,
which results in immunosuppression. As the
number of CD4+ T lymphocytes is reduced, the
affected patient becomes increasingly vulnera-
ble to opportunistic infections, which can over-
whelm the patient’s compromised defense
systems. Pneumocystis carinii pneumonia is the
most common serious opportunistic infection,
though there are many others, including pul-
monary tuberculosis. AIDS was at first defined
solely by clinical conditions, but a 1993 revi-
sion of the classification system by the CDC
redefined the stages of HIV infection in terms of
three ranges of CD4+ T-lymphocyte counts and
three groups of clinical manifestations, set out
in a nine-cell matrix.25 These nine categories
range from asymptomatic HIV infection or per-
sistent generalized lymphadenopathy with a
CD4+ T-cell count of 500/μl or more at the mild
end of the scale, to the diagnosis of 1 of 25
AIDS-indicator clinical conditions plus a CD4+
T-cell count of 200/μl or less at the severe end.
Dentally related conditions listed among the
clinical diseases that are considered part of
the AIDS diagnosis include oropharyngeal
 10 The Healthy Dental Practice: Infection Control and Mercury Safety 141
candidiasis, oral hairy leukoplakia, chronic her-
pes simplex, and Kaposi’s sarcoma.
The disease we call AIDS is the “finale in a
progressive process of immunologic deficit
mediated by the virus.”76 The primary epidemi-
ology of HIV infection has been well described
in terms of risk factors and modes of transmis-
sion, although research is still needed on the
dynamics of transmission and infection. The
average time between infection with HIV virus
and the onset of AIDS-like symptoms is esti-
mated to be 10 years,76 so that HIV disease is
like a “time bomb.” HIV infection is diagnosed
when results of a serologic test are positive; the
condition becomes AIDS when a low CD4+
count is found in combination with one of the
AIDS-indicator clinical conditions.
The principal mode of transmission in North
America is homosexual contact among men fol-
lowed by intravenous drug injection with con-
taminated needles and heterosexual contact.106
There are a small number of cases in which
transmission has occurred perinatally (i.e., birth
of an infant to an infected mother) and from
transfusion with infected blood (e.g., as with
the late tennis player Arthur Ashe in the early
1990s). The principal mode of transmission in
poor countries is heterosexual contact. Despite
the publicity given to the risk associated with
certain sexual and drug-use activities, behav-
ioral change among the highest-risk groups
does not come easily. The epidemic is increas-
ingly affecting women, minorities, the poor,
and heterosexual persons.55
In the early days of the AIDS epidemic in
North America, diagnosis with HIV infection
meant virtually certain death within a few years.
BOX 10-1 Global Extent of AIDS/HIV Infection in December 2002118
●
Globally, 42 million people, 38.6 million adults and 3.2
million children, are estimated to be living with AIDS/HIV.
●
In 2002, 70% of these cases were in sub-Saharan
Africa and another 14% in South and Southeast Asia.
●
In 2002, HIV-associated illnesses caused the death of
3.1 million people, including 610,000 children under
age 15.
●
Women are becoming increasingly affected. Women
accounted for half of the HIV-infected adults and half
of the HIV-related deaths in 2002.
Drug therapy developed quickly, and protease
inhibitors showed some good effects. A few
years later treatment evolved into the “cocktail”
of antiretroviral drugs known as highly active
antiretroviral therapy (HAART), which greatly
extended life expectancy and has allowed many
HIV-positive persons to live more or less nor-
mal lives. HAART has probably reduced much
of the fear that surrounded HIV infection a gen-
eration ago, which may or may not be a good
thing. In any event, the success of HAART
should not blind us to the fact that AIDS is a
pandemic, a global epidemic of massive pro-
portions that is devastating a number of poor
countries. HAART is far too expensive to be used
widely in these poor countries at market prices.
Box 10-1, which shows some of the global data
for 2002, indicates the enormity of the HIV pan-
demic.
Figures for the United States are not as mind
boggling as the global data but still tell us that
AIDS is a major epidemic.106 At the end of 2002,
there had been 501,669 deaths from AIDS in
the United States, including 5315 children
under age 15. The death count had increased
39% over 6 years. The cumulative number of
cases reported since the beginning of the epi-
demic in the United States was 886,575. The
number of adults and adolescents living
with AIDS was 384,906, an increase of 73%
over a 6-year period. No one knows how many
people are infected with HIV who have not yet
been diagnosed, but it is likely to be over a
million. It is because of this large number of
undiagnosed HIV carriers that the estimates
of the growth of the epidemic are ominous.
Development of successful vaccines is not
●
Newly infected persons during 2002 included 5
million adults and 800,000 children under age 15.
●
The main mode of transmission in North America and
Europe is sexual contact between men, intravenous
drug use is second, and sexual relations between
heterosexual individuals is third. In sub-Saharan Africa,
transmission is almost entirely from heterosexual
contact.
142 Dental Practice
considered likely, and HAART treatment is
expensive, so control of the epidemic falls back
on the toughest measure of all: education to
control risky human behavior.
AIDS presents some paradoxes. For example,
despite the “time-bomb” implications of the
extent of current infection and thus the near cer-
tainty of the continued growth of the epidemic,
the responsible virus is really quite delicate and
hard to transmit. Although dental professionals
are at relatively greater risk than average mem-
bers of the public because of their close contact
with saliva and blood, they still have an
extremely low risk of occupational exposure.56
A small number of health care workers have
become HIV infected through occupational
exposure, but the risk of seroconversion even
after needlestick exposure to HIV-infected
blood is still only about 1 in 200.111
A possible case of HIV transmission from an
infected dentist in Florida to a patient was
reported in 1990; the dentist died soon after the
patient was diagnosed. In this case the patient
had two maxillary third molars removed by the
dentist. She reported pharyngitis 4 months later
and had oral candidiasis 17 months later. Two
years after the extractions, she was seropositive
for HIV antibody and was diagnosed with
P. carinii pneumonia. The dentist was reported
to have worn gloves and mask throughout the
procedure, and from the patient’s statement
there was no evidence of exposure to the den-
tist’s blood. There were similar DNA sequences
in peripheral blood mononuclear cells of both
dentist and patient, like those found in many
cases that have been epidemiologically linked.
Soon afterward, evidence emerged that eight
other patients treated in this practice were
HIV infected, and there were strong indications
that the dentist was the source of infection for
at least five of them.26 The ADA responded
quickly to this disclosure in early 1991 with an
interim policy that HIV-infected dentists should
not perform invasive procedures or should dis-
close their seropositive status to their patients.69
The CDC closed the case in 1992 without being
able to reach firm conclusions about whether
the dentist infected his patients.
Since then, the CDC has issued guidelines
that place some limitations on HIV-infected
practitioners, mostly restricting the perform-
ance of major invasive procedures. Some states
have a legal requirement that an HIV-infected
practitioner disclose this status to the patient,
although usually this does not mean that the
practitioner is not permitted to perform a given
procedure.11 Again, it can be seen that the basis
for these requirements is the effectiveness of the
standard precautions.
Oral Manifestations of HIV Infection
All dental professionals should be thoroughly
familiar with the oral manifestations of
HIV infection. The principal signs are oral can-
didiasis, oral hairy leukoplakia, and Kaposi’s
sarcoma, although periodontal conditions are
frequently bad in persons with advanced
immunosuppression117 and a number of less
common disease entities are also found.89 The
details of these conditions are covered thor-
oughly in oral pathology texts50 and workshop
proceedings.81 The three principal signs are
described only briefly here.
1. Oral candidiasis: A fungal infection, can-
didiasis (called candidosis in Britain) usu-
ally presents as a semi-adherent white
plaque on the palate, although glossitis
and angular stomatitis forms are not
uncommon. The plaques can be sore, and
they are very common among HIV-posi-
tive individuals. An excellent presentation
by Pindborg on the diagnosis and treat-
ment of oral candidiasis is available.77
2. Oral hairy leukoplakia: In a study of 375
homosexual males who either had AIDS
or were considered at risk for the disease,
28% presented with oral hairy leuko-
plakia. The lesions appeared most com-
monly on the lateral surface of the
tongue, with wide variation in the size,
severity, and surface characteristics.88 The
condition is highly predictive of the
future development of AIDS. In a longitu-
dinal study of a group with oral hairy
leukoplakia, survival analysis showed that
the probability of AIDS’ developing in the
patients was 48% after 16 months and
83% after 31 months.49
3. Kaposi’s sarcoma: Kaposi’s sarcoma is diag-
nostic for AIDS and is found in some
20%-34% of AIDS patients.42 The oral cav-
ity may be the first or only site of the
lesion. The most common intraoral site is
the palate. The pathogenesis of the disorder
 10 The Healthy Dental Practice: Infection Control and Mercury Safety 143
is still not well understood, nor is its inter-
action with HIV infection. Treatment is
required because of functional impair-
ment, pain, or bleeding, or for cosmetic
reasons.
The particularly distressing condition of
pediatric AIDS, in which HIV is transmitted
from an infected mother, appears to be on the
increase. Recognition can be difficult because of
the varied presentation of the condition, but the
most common oral findings include candidia-
sis, parotid salivary gland enlargement, and her-
petic infections.94
HEPATITIS B AND C
Hepatitis is a far more prevalent disease than
HIV, both worldwide and in the United States.
The CDC estimates that 45% of the world’s
population live in areas of high prevalence,
43% in areas of moderate prevalence, and only
12% in areas of low prevalence.107 Globally, the
World Health Organization estimates that 2 bil-
lion people have been infected with HBV and
that currently some 350 million people have
chronic infection.119 In poor countries, 8%-10%
of the total population is chronically infected,
and in these regions liver cancer, a result of
chronic HBV infection, is among the top three
causes of death in men.119 By contrast, fewer
than 1% of the population in high-income
countries is chronically infected.
The United States and other high-income
nations are areas of low prevalence, although
there are still around 80,000 new infections per
year in the United States.108 Hepatitis B is pri-
marily a disease of young adults in the United
States (peak age for new infections is 20-29
years), whereas in poor countries it is a child-
hood disease. Both HBV and HCV are transmit-
ted by contact with infected blood, so the
primary transmission routes are:
●
Sexual contact, both homosexual and het-
erosexual, especially unprotected sex
●
Sharing of infected needles
●
Perinatal transmission to an infant born to
an infected mother
Although the case fatality rate from HBV
infection is low (0.5%-1%) and most infected
people recover completely in due course, a sig-
nificant number of people develop chronic
infection. It is in these chronically infected peo-
ple that the most serious sequelae are found.
HBV carriers are at risk of long-term sequelae
such as chronic liver disease, cirrhosis, and liver
cancer, though a more common outcome than
death is severe and usually lifelong debilitation.
The risk of becoming a chronic carrier of HBV
varies with age at first infection. Among those
first infected as young children, 30%-90%
develop chronic infection, whereas among those
who were adults when first infected only 2%-
10% do. Chronic infection can be asympto-
matic, but 15%-25% of this group can die
prematurely from cirrhosis or liver cancer. The
CDC estimates that there are some 150 deaths
per year from acute hepatitis, although there are
around 5000 deaths each year from chronic liver
disease. Although the good news is that the
number of new infections has been dropping in
recent years (Fig. 10-1), the bad news is that
there are still 1.25 million persons chronically
infected with HBV and 2.7 million HCV-infected
persons in the United States.108
Signs and symptoms of hepatitis B and C are
very general (fatigue, abdominal pain, loss of
appetite, intermittent nausea and vomiting,
jaundice), and hence the condition can easily
be misdiagnosed. Health care workers are at
higher risk than the general population because
of their likely contact with chronic carriers. The
CDC has estimated that there are some 18,000
infections each year among health care workers
in the United States, the majority through expo-
sure to infected blood. Blood and serous fluids
have the highest concentration of HBV in
infected persons; the concentration in saliva is a
little lower. However one looks at it, hepatitis B
is a disease to be taken seriously.
Fig. 10-1 shows the annual incidence of HBV
and HCV infection in the United States from
1980 to 2001. The prevalence of tuberculosis,
another infectious disease that has caused con-
cern in dental practices, has been included in
this graphic. The drop in incidence of HBV
infection through the 1990s is thought to be
due partly to the effectiveness of the HBV vac-
cine but mostly to behavioral change among
risk groups (injection drug users, the indiscrimi-
nately sexually active, and immigrants from
high-prevalence areas) because of their fear of
AIDS.
The most insidious aspect of HBV infection
is the relative ease with which carriers can
144 Dental Practice

14

12
Cases per 100,000 population

10

2 Hepatitis B
Hepatitis C
TB
0
1979 1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 2001
Year
Fig. 10-1 Incidence of hepatitis B (HBV) and hepatitis C (HCV), and prevalence of tuberculosis in the United States,
1980-2001.107,108

inadvertently transmit the disease to anyone cautions were widely used. The greatest risk of
with whom they come in contact in day-to-day infection in the dental office clearly comes from
life. The worst reported instance of an infected the undiagnosed carrier, whether it be a patient,
dentist’s inadvertently transmitting HBV to his the dentist, or one of the office staff.34
patients was in Indiana in 1984-85. Nine Hepatitis viruses A, B, C, D, and E have been
patients of a dentist in a rural county came down identified. Some 90% of non-A, non-B viruses
with HBV infection within 2-5 months after are now recognized as HCV. The designation
being treated by the dentist, a vastly higher inci- non-A, non-B came after more stringent screen-
dence than had previously been reported in the ing of blood donors in the 1970s resulted in a
area. Two of the patients died. Although the den- sharp decrease in the incidence of hepatitis B
tist had never had hepatitis symptoms, serum due to blood transfusion; the non-A, non-B des-
tests showed that he was probably a carrier.92 ignation was given to the type of hepatitis that
In contrast to the AIDS virus, HBV is hardy continued to occur after blood transfusion
and capable of being transmitted much more despite the new screening program. HCV was
readily via percutaneous and nonpercutaneous identified as the causative agent in 1989.119
routes.33 To heighten the contrast, it was HCV infection has an insidious onset, and like
reported in 1989 that whereas 15 health care HBV infection it can be easily missed in its early
workers had become seropositive for HIV over stages. Only some patients become sympto-
the previous 7 years in the absence of outside matic (symptoms are similar to those for HBV
risk factors, a total of between 1750 and 2100 infection); the majority of infected persons
health care providers had died from complica- show no symptoms. It is estimated that 2.7 mil-
tions associated with HBV infection over the lion Americans are infected with HCV, with
same period.64 Because carrier states of HBV are infection more common in minority popula-
not uncommon, with only 20% of infections tions.110 Some 85% of infected persons develop
being recognized, the patient history can be of chronic infection. As with HBV, transmission of
little value for dental practitioners.33 The risk of HCV is by infected blood, so the main routes are
contracting HBV infection has been estimated sexual contact, both heterosexual and homo-
to be 3-10 times greater for dentists than for the sexual; use of infected needles; and perinatal
general population,3,116 although those esti- infection. Also as with HBV infection, health
mates came from the days before standard pre- care workers are considered to be at higher risk
 10 The Healthy Dental Practice: Infection Control and Mercury Safety 145
than the general population. Unlike for HBV,
however, no vaccine has yet been developed for
HCV. Hepatitis C is responsible for 8,000-
10,000 deaths from chronic liver disease annu-
ally in the United States (i.e., more than from
HBV infection), and without effective interven-
tion that number is expected to grow over the
next 10-20 years.
The barrier precautions (gloves, masks, and
eyewear) and sterilization procedures for pre-
venting HCV transmission are the same as those
for preventing HBV transmission. However,
unlike with AIDS, there has been an effective
vaccine against HBV since 1982.119 Since that
time, both the CDC and the ADA have strongly
recommended immunization against HBV for
all dental office staff who contact patients, and
as described earlier, OSHA regulations now
require that dentists provide HBV vaccination
for their office staff. Immunity status is readily
tested. For most, immunization through a series
of three injections over 6 months will be
required. Vaccination is specific to HBV and
does not protect against HCV or other non-A,
non-B forms of hepatitis.79
Dentists have responded well to the need to
ensure their immune status to HBV. Among
dentist participants in the ADA’s health screen-
ing at the annual meeting, those reporting vac-
cination increased from 22% in 1983 to 84% in
1992, and the number whose blood tests
showed current infection (i.e., presence of the
HBV surface antigen) dropped from 14% to 9%
over the same period. Chronic carrier status
(i.e., positive result for both the HBV surface
antigen and core antigen) dropped among
dentists from 0.95% in 1983 to 0.25% in
1992.30 Even higher rates of immunization
were reported by a national survey of dental
personnel in Britain.90 Vaccination is more
common among younger than among older
dentists, so in time virtually all dental person-
nel should be immune to HBV.
PUBLIC AND PROFESSIONAL
PERCEPTIONS OF INFECTIOUS
DISEASES
As the public has come to accept the existence of
an HIV epidemic, attitudes of dentists toward
treating infected people have also matured. Not
surprisingly, dentists in a number of countries
demonstrated ambivalent attitudes toward
treating infected patients, especially in the
early days of the epidemic.44,83,87,101 Treating
infected patients was seen as a professional
responsibility fulfilled reluctantly, and many
clearly would have preferred not to treat
infected patients.20,57,84 With the adoption of
standard precautions and the realization that
adherence to them greatly reduces the risk of
transmission of HIV, HBV, and HCV, rational
fears on the part of dentists seem to be allayed.
However, there are still a lot of dark, irrational
fears and anxieties,20,68,86 especially of HIV
infection, that do not abate with continuing
education and evidence of extremely low risk of
transmission. A general willingness to treat
HIV-positive patients was expressed by two-
thirds of dentists in a New York City study in the
early 1990s, but this proportion dropped when
the patients concerned were not patients of
record in the practice.85 HIV-infected patients,
who used to be referred to clinics dedicated to
treating them, are increasingly feeling comfort-
able in general dentists’ offices.19 As noted ear-
lier in this chapter, dentists do not have the legal
right to turn away prospective patients who are,
or may be, HIV or HBV infected. By the same
token, with standard precautions there is no
need for anxiety when treating such patients.
Surveys in the mid-1980s found variable
adherence to infection-control procedures in
the dental office44; some dentists were appar-
ently slow to accept that they were at risk
without them. Dental professionals who
accepted that some of their patients were proba-
bly infected were more likely to adhere to
the recommendations,46 and educational pro-
grams for dental personnel were effective in
improving adherence to these procedures.39,45
Attitudes and infection-control practices
appeared to move forward considerably in the
late 1980s, however, because a national survey
of general dentists in 1990 found virtually uni-
versal acceptance of the need for infection-con-
trol procedures in the dental office.84 These
advances in attitudes and practice continued for
dentists through the 1990s,31,47 although it has
been pointed out that, while use of standard
precautions has become common, the poor
communication between dentists and HIV-
infected patients has changed little.51 A study of
hygienists in Mississippi also disclosed that
146 Dental Practice
their attitudes and beliefs had not kept pace
with modern knowledge, so there is still appar-
ently a need for continuing education on infec-
tion control.37
HIV ISSUES IN DENTAL PRACTICE
AND DENTAL EDUCATION
The legal implications of cross-infection con-
tinue to evolve, and all dental practitioners need
to be constantly aware of them. HIV-infected
dentists are in a particularly difficult position.
A number of states have responded to public
clamor with laws restricting the rights of
infected dentists to practice. Many interpret
these laws as overreaction, although in states
without them the dentist’s legal obligation to
tell patients and staff that he or she or a staff
member is HIV- or HBV-infected is not clear. If
the dentist does so, then the ensuing hysteria
would probably force the practice to close; if the
dentist does not, he or she is probably liable
should a patient become infected.61
On the other hand, dentists have a clear legal
obligation, under the Americans with Disabilities
Act of 1990, not to deny treatment to a patient
solely on the grounds of the patient’s infection.
This became clear in a 1997 U.S. District Court
judgment against a dentist who, it was alleged,
denied treatment to a patient solely on the
grounds of the patient’s HIV status.36 The dentist
appealed, but the U.S. Court of Appeals reaf-
firmed the District Court’s decision. The ruling
was based on the evidence that standard precau-
tions reduce the risk of transmission to extremely
low levels.
Willingness to treat HIV-infected patients is
an issue that organized dentistry, and the dental
schools in their curricula, should deal with
vigorously. The ADA has included in its code of
ethics (see Chapter 3) the statement that refusal
to treat an HIV-infected patient, solely on those
grounds, is unethical. As just discussed, it is also
illegal. It is a position that also makes little
sense because (1) the risk of transmission of
HIV from patient to dentist, as already dis-
cussed, is extremely low when the dentist is
using standard precautions, and (2) many den-
tists already have treated HIV-infected persons
without knowing it.
The fact remains that a level of anxiety
persists about treating infected patients, espe-
cially HIV-infected patients. Some dentists are
adamant that they do not have an ethical
responsibility to treat HIV-positive patients.86
These dentists cite a lack of confidence in stan-
dard precautions and concerns about what will
happen to their practices if it becomes known
that HIV-positive patients are treated there. The
majority of dentists accept their ethical respon-
sibility to treat infected patients, though most
would rather not do so if they had the choice.20
In a 1991 national survey of senior dental stu-
dents, 76% agreed that an ethical responsibility
existed to treat infected patients, although 54%
admitted to having some fear about treating
infected patients and 53% would prefer not
to do so if given the choice.96 AIDS clinics
appeared in a number of major cities, manned
by dental practitioners whose commitment to
equality of care for all represented the highest
degree of professionalism. However, by the end
of the twentieth century the trend was toward
“mainstreaming” (i.e., treatment in private den-
tal offices rather than in segregated facilities).
The issues raised in dental education by the
AIDS epidemic are many and will take years to
become resolved. Two questions that readily
arise are the following:
1. Should an HIV-positive student applicant
be admitted to dental school?
2. What is the dental school’s obligation if a
student becomes HIV positive in the
course of clinical duties?
Some experience in these matters has accu-
mulated. There are several documented cases of
students who were identified as HIV positive
during their studies and after they had begun
treating patients,35,52,100 and at least one docu-
mented case of a faculty member who died of
AIDS.23 In each instance the experience was dis-
ruptive for all concerned. In the cases of the stu-
dents, what followed was similar in each
school. The student was immediately removed
from patient contact, patients treated by the stu-
dent were offered free testing and counseling,
and confidentiality of the student’s identity was
maintained in the face of intense media pres-
sure. Reviews were made of the student’s com-
pliance with infection-control procedures and
of the school’s procedures for sterilizing instru-
ments. Extensive meetings of school adminis-
tration with faculty and students were held to
explain the actions taken and the reason for
 10 The Healthy Dental Practice: Infection Control and Mercury Safety 147
them. (None of the patients tested was seropos-
itive.) At least one of the students concerned
completed his dental degree, carrying out his
remaining required clinical procedures on
patients known to be HIV infected.52
Dental schools should have clear policies on
these issues and an established plan of action to
be followed when an incident arises. There are
many implications to whatever policies are
adopted, but experience has shown that the worst
thing to do is to stick our collective heads in the
sand and hope that nothing unpleasant will hap-
pen with respect to HIV in dental educational set-
tings. Almost certainly the situations described
earlier will occur at other schools, and the
schools should be ready to handle the situation.
The AIDS epidemic has already had a dra-
matic effect on the practice of dentistry, and it
will continue to affect it in complex ways for the
foreseeable future. As was said the day after the
first nuclear bomb was dropped on Hiroshima
in 1945, nothing will ever be the same again.
DENTAL UNIT WATERLINES
There is evidence that the water used in the den-
tal operatory for cooling, irrigation, and flush-
ing can be infected, sometimes quite heavily
infected.38 Certain microbial species can form
biofilms in the waterlines, and small bits of
biofilm can break off and infect the water going
into the patient’s mouth. Human pathogens
have been isolated from this water, including
Legionella pneumophila, the causative organism
for Legionnaires’ disease. Although outbreaks of
Legionnaires’ disease occur periodically, none
has been associated with dental procedures,
and there are no specific recommendations for
preventing L. pneumophila infection in dental
practice. However, given the increasing number
of immunologically compromised patients
now being seen in dental practices, the possibil-
ity of infection is clear.
There is no good research base from which to
provide recommendations on how to deal with
the problem. The CDC’s recommendations
include the use of sterile water for invasive pro-
cedures and regular flushing of the water-
lines.105 The CDC also states, however, that
although these procedures help to reduce the
numbers of microorganisms in the water they
do not reduce biofilm formation.
In 1995 the ADA set a goal of having equip-
ment available by the year 2000 that would
provide unfiltered water with no more than
200 colony-forming units/ml.10 This is the
same standard that applies to kidney dialysis
machines. Although some advances have been
made, progress toward this goal is slow.
An issue related to waterline infection is back-
flow. Cross-connection is the name given to the
link by which contaminated materials may enter
a public water supply when the pressure from
the polluted source exceeds the pressure of the
water supply. The risk of such an occurrence,
already extremely low, is reduced even further
when backflow prevention devices, or antiretrac-
tion valves, are used to prevent back-siphonage
of contaminated fluids. Although a cross-con-
nection is also theoretically possible through the
high-speed handpiece and the air and water
syringe, this risk, too, is extremely low and has
not yet been documented.10
Much of the concern expressed about back-
flow relates to the chance of HIV, HBV, or HCV
infection through this route, but this possibility
is close enough to zero, because none of these
viruses is transmitted through contaminated
water. The use of self-contained water systems in
the dental office—that is, water systems not
connected to the public water supply—is a rec-
ommended measure to reduce any possible risk
even further.
DENTAL AMALGAM: SAFETY
AND ENVIRONMENTAL ISSUES
Amalgam restorations have been used in dental
practice since the mid-nineteenth century, and
it would be impossible to calculate how many
have been placed since then. Today, millions of
people around the world are carrying amalgam
restorations around in their mouths without
apparent ill effects. Amalgam use has lasted so
long because amalgam is stable in the compli-
cated oral environment, it is easy to handle, and
it is relatively cheap. Even with new composite
and bonding materials now in use, amalgam
remains a basic restorative material. However,
the toxic properties of mercury have been
known for years, and with current environmen-
tal sensitivities some observers have charged
that it is no longer conscionable to use a mer-
cury compound in the human mouth.
148 Dental Practice
Mercury vapor is released from amalgams,
and average daily intake of mercury from amal-
gam restorations is estimated to be 1.2-1.3 mcg
when tested subjects have seven or eight restora-
tions.66,97 This amount constitutes 6%-12% of
total mercury intake from all sources.67 Earlier
estimates of up to 20 mcg/day from amal-
gams112 have been criticized as being some 16
times too high because of the failure to account
for the difference between the flow rate of the
mercury vapor detector and that of human res-
piration.67 However, opponents of amalgam
use still insist that exposure to mercury from
dental amalgams exceeds the sum of exposures
from all other sources.62
The evidence against the use of amalgam
restorations on health grounds is largely circum-
stantial. Among patients, intraoral measurements
of mercury vapor show higher readings in
adults with amalgam restorations than in those
without, and the differential is higher after chew-
ing.99,112,113 Computer simulations based on
these data have led to the estimate that long-term
inhalation of mercury vapor from restorations
results in an increasing mercury burden in the tis-
sues.114 In animal studies deleterious effects on
brain tissue and intestinal microbial flora have
been reported from amalgams.63 In humans
blood mercury levels have been correlated with
the number and surface area of amalgam restora-
tions, and have been measured as significantly
lower in people without amalgam restora-
tions.1,59,97 However, raised levels of mercury in
urine could not be demonstrated in child patients
after a single session of restorative dentistry,75
although this finding could have resulted from
the relatively small amounts of amalgam used.
Dentists generally have levels of urinary mer-
cury that are higher than those found in the
general population but are still well below
safety limits. Mercury levels among dentists
attending the ADA annual session show wide
variability but generally are higher in dentists
who have greater exposure to mercury. Thus
higher levels are seen in older dentists and in
generalists rather than specialists and are
related to the number of amalgams placed,
form of amalgam preparation, and type of heat-
ing and cooling system in the office. Dentists in
the New England and mid-Atlantic regions, on
average, had twice the urinary mercury levels
found in West Coast dentists.71 Swedish studies
have shown higher urinary mercury levels in
dental personnel than in nondental controls,
although all values were well below those set in
occupational health standards.73,74
Because one of the outcomes of mercury tox-
icity is neurologic damage, some studies had
looked specifically for neurologic syndromes
related to amalgam restorations. The evidence
here is weak. One researcher concluded that the
prevalence of multiple sclerosis was related to
the use of amalgam restorations,54 although the
evidence presented was so broad that this con-
clusion was hard to accept. (The evidence pre-
sented was ecologic: there are more amalgams
placed in the northern United States than in the
south, and there is also more multiple sclerosis
in the north. The prime weakness in this argu-
ment is that the people with the disease are not
necessarily the people with the restorations.)
Evidence of neurologic damage has been
reported in some dentists with exceptionally
high mercury tissue levels,91 and there are a few
reports of mental distress in dentists and
patients supposedly resulting from exposure to
mercury.93,95 Other reports have concluded
that the symptoms reported by patients who
believed that amalgams were making them sick
were of psychosomatic origin.60
Widespread media publicity has been given
to the results of animal studies with amalgam.
Reports on studies of sheep, for example, have
concluded that mercury inhaled from amal-
gams placed in pregnant ewes appears in the
fetal circulation within 2 days.115 Critics con-
tend that the sheep, a ruminant, is a poor model
in which to study mercury inhalation.
The validity of a number of these studies,
involving both humans and animals, remains a
subject of debate; firm conclusions are hard to
reach from them. Critical reviews of the literature
have concluded that mercury from amalgam
restorations does find its way into human tis-
sues,27,41,58,89 although these same reviewers all
consider there to be no evidence for ill effects in
humans from the amounts in question. For
example, no difference in lymphocyte levels
could be found in comparisons between persons
with amalgam restorations and those without.67
Subsequent studies examining the potential
effects of amalgam on human health have all
concluded that amalgam use has no adverse
consequences.2,21,22 But in a debate that some-
 10 The Healthy Dental Practice: Infection Control and Mercury Safety 149
times has overtones of that surrounding water
fluoridation (see Chapter 25), not every single
health hypothesis can be tested, and the question
of whether subtle side effects exist would require
a lot of additional research to be fully answered.
Literature reviews have also concluded that bad
health effects result from amalgams,63,78 but oth-
ers have concluded that mercury from amalgams
had no effect on Alzheimer’s disease.28 The issue
has even provoked a spirited response from the
antiquackery watchdog group the National
Council Against Health Fraud,72 which came out
firmly in favor of amalgam restorations.
By the early 1990s the issue had become an
emotional debate that spilled over from scien-
tific discussions into the public arena, with
numerous lawsuits filed by antiamalgam
activists. The ADA has consistently maintained
its support for the use of amalgams on the
grounds that there are no substantiated reports
of ill health to humans resulting from their use.
The courts have agreed. Over 2 years beginning
in June 2001, 32 very similar amalgam-related
complaints were filed in different parts of
the United States. All were dismissed.24 Bills to
ban amalgams have also been introduced in
Congress and some state legislatures. All have
alleged environmental pollution from amal-
gam waste and adverse health effects among
people with amalgams. The ADA has vigorously
and successfully campaigned against these bills.
The amalgam health issue is not new in ADA
circles; a 1971 review concluded that normal
handling of mercury in practice does not present
a threat to patients, although it can present a
threat to dental personnel if precautions are not
taken.82 This review led to formulation of the
ADA’s first set of 15 recommendations on mer-
cury hygiene in 1974.12 In its own review of the
literature, the ADA concluded that there was no
need to remove amalgams from patients except
in the rare cases of mercury allergy.14 A second
set of recommendations on mercury hygiene was
issued in 1984, rather more stringent than the
first edition, which included reference to OSHA
requirements for disposal of scrap amalgam.15
Further updates of these recommendations fol-
lowed in 19998 and 2003,9 and the ADA will no
doubt continue to give this issue close attention.
The ADA derided the claims that removal of
amalgams could improve the condition of mul-
tiple sclerosis sufferers as “a cruel hoax”17 and
made a strong statement with an advisory
opinion in the code of ethics, which states the
following:
The removal of amalgam restorations from the non-allergenic
patient for the alleged purpose of removing toxic substances
from the body, when such treatment is performed solely at the
recommendation or suggestion of the dentist, is improper
and unethical.7
It is clear that research and public inquiry on
this issue should continue, though as with many
environmental questions the determination of
cause and effect is extraordinarily difficult.
Symptoms of mercury toxicity are general in
nature, similar to those of dozens of other med-
ical conditions. Threshold limits in occupational
medicine are at best broad estimates, and extrap-
olation from animal studies to human condi-
tions is always difficult. Humans are also exposed
to environmental mercury from other sources,
such as organic mercury from seafood. As was
mentioned earlier, mercury from amalgams con-
stitutes only some 6%-12% of daily intake for
adults with amalgam restorations. Improvements
in alternative restorative materials are neverthe-
less to be encouraged, and the sealants and mini-
mum-preparation restoration procedures that are
evolving (see Chapter 27) are increasingly appro-
priate for restorations in children.43 The mercury
issue can be expected to diminish over time as
composites and sealants replace amalgams in
children and complex restorations in young peo-
ple become increasingly uncommon.40
The U.S. Public Health Service conducted an
exhaustive review of amalgam safety in 1993.109
The review concluded that amalgam use was
declining as caries experience diminished and
other materials were used more often. However,
there was an appropriate note of caution. The
committee (which could hardly be accused of
bias because it did not contain a dentist) con-
cluded that, although there was no clear evi-
dence that amalgam caused harm in humans
apart from rare allergic reactions, the very
paucity of reliable studies required that further
investigation of the issue should continue. As
with all issues in infection control and environ-
mental safety, however, the dental profession
cannot determine policy by itself. Although the
dental profession should act as a leader, both
these subjects are public health issues and must
be handled as such.
150 Dental Practice
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 11 Reading the Dental Literature
TEXTBOOKS AND PEER-REVIEWED
JOURNALS
Peer Review
Judging the Quality of a Journal
CRITICAL READING—EVALUATING THE
QUALITY OF A PUBLISHED PAPER
Hierarchy of the Quality of Information
The literature is the generic name given to the
body of writing in books, journals, reports, and
other sources that makes up the sum of knowl-
edge in a branch of science. In the case of
dentistry we refer to the dental literature.
However, the literature is more than just our
compendium of knowledge and our scientific
base; it is our very identity. It defines who we are
and what we do; it charts the progress of den-
tistry to its present status and provides guide-
lines for future directions.
Technologic and social developments, in
dentistry as elsewhere, are proceeding at a speed
that can be both bewildering and overwhelm-
ing. Although dental and dental hygiene gradu-
ates learn enough in professional school to
begin practice, “keeping up” is absolutely essen-
tial for professional growth. Attendance at con-
tinuing education courses is one way to do so
(such attendance is required in most states), but
the literature is the primary source of new
knowledge. Therefore it follows that dentists
and hygienists must keep familiar with those
sections of the literature that most concern
them if they are to function properly. To do this,
they need to be able to locate the literature they
need and read it critically; they need to distin-
guish front-line from mediocre journals and be
aware of how to distinguish good from poor
research. Acquiring these skills requires some
time and practice, but confidence with them
will pay off in helping practitioners use their
154
Criteria for Judging the Quality of an Individual
Paper
FINDING THE REPORTS YOU NEED IN THE
LITERATURE
time efficiently while they grow professionally.
Professional training, unfortunately, does not
usually include critical reading. The usual pro-
gression begins with accepting the veracity of
reports unquestioningly and without conscious
thought, because “if it weren’t true, it wouldn’t
be printed.” After being misled a few times,
readers can become increasingly skeptical. In
the extreme, they can move full circle from
believing everything they read to believing
nothing. The ideal course is between the two
extremes, somewhere between blind acceptance
and blanket mistrust.
This is the first of two chapters on how to
efficiently locate and interpret information that
is needed for effective clinical practice. This
chapter deals with assessing the quality of an
individual report in the literature, whereas
Chapter 12 is devoted to evidence-based den-
tistry and assessment of a body of literature to
determine best clinical practices.
TEXTBOOKS AND PEER-REVIEWED
JOURNALS
Textbooks are the most familiar source of infor-
mation for students. Although good books may
be the first source to be consulted on a subject,
books can soon become dated. The copy a stu-
dent buys from the bookshop may be new, but
if it was published 10 years ago then at least
parts of it risk being obsolete. That proviso

accepted, the best textbooks present the state of
the science, at least at the date of publication, as
well as a sound foundation on which to build
further information.
Journals are the basic source of current infor-
mation in any science-based field, dentistry
included. The number of journals in dentistry,
as in most other disciplines, has proliferated in
recent years. It is virtually impossible for anyone
to keep up with all journals, so selectivity is
needed. There are good journals and not-so-
good ones, and there are some clues to picking
which is which. The most basic is that good
journals are all peer reviewed.
Peer Review
Peer review means that manuscripts, when first
received by the journal editor, are sent out to be
reviewed by several experts in the subject area
of the manuscript. Usually two reviewers are
selected, sometimes more, and the identity of
the reviewers is concealed from the authors to
promote candid reviews. Some journals, though
not all, also mask the identity of the authors
from the reviewers in an effort to remove any
bias from the reviewers’ judgment. The review-
ers’ task is to assess the manuscript critically for
the quality of its science, its logic, its manner of
presentation, and any other feature that might
reflect on its value in the literature. Poor-quality
manuscripts can be rejected outright at this
stage or returned to the authors for revision if
the papers are basically sound but have room
for improvement. Most articles published in
journals have been returned to the authors for
revisions at least once prior to acceptance. Many
prestigious journals, such as the New England
Journal of Medicine, reject far more manuscripts
than they publish; their reviewing standards are
extremely rigorous. The top dental journals
publish well under half of the manuscripts they
receive.
Peer review is a system that has evolved
through the years, and there is no question that
it has served to greatly elevate the standards of
published material. However, it does have some
limitations. For example, the process can suffer
when the reviewers chosen are inappropriate,
either because they are not sufficiently expert in
the field of study or because their own preju-
dices get in the way of an objective review. More
common are reviewers who simply do not give
11 Reading the Dental Literature 155
a manuscript the attention it deserves. An inher-
ent problem is the tendency of the peer-review
process to inhibit original research or creativity
and to push imaginative thoughts into a safe
middle ground. On balance, however, peer
review has served to greatly elevate the quality
of the literature.
Judging the Quality of a Journal
The first step in judging a journal’s quality is to
find out whether it is peer reviewed or not. Some
provide this information in their instructions to
contributors, which journals publish regularly
and which can usually be found on the journal’s
website. The second thing to find out is the jour-
nal’s sponsorship: who puts it out? Here are four
broad categories of sponsorship:
A Learned Society Learned societies frequently
present the best and most important research
papers—their reason for existing, after all, is to
promote and disseminate research findings.
Some, like the International Association for
Dental Research, which publishes the Journal of
Dental Research, Critical Reviews in Oral Biology
and Medicine, and Advances in Dental Research,
promote dental research in all fields; others
advance research in specialized or semispecial-
ized areas. Journals published by learned soci-
eties are invariably peer reviewed and have a
strong emphasis on scientific rigor. These jour-
nals are characterized by a straightforward for-
mat with a relative absence of advertising, a
strong editorial board, and explicit instructions
to contributors. On the down side, a relatively
small circulation to a specialized group often
makes them expensive.
A Professional Organization A professional
organization is a dental or dental hygiene associ-
ation, a specialty society, or any other profes-
sional group. The best journals in this category,
such as the New England Journal of Medicine,
British Medical Journal, and Journal of the American
Medical Association, rank among the most presti-
gious in biomedicine. The majority of journals in
this group are peer reviewed. In contrast to the
journals published by learned societies, these can
show some bias in choice of material: there can
be a tendency to publish papers favorable to the
organization’s views and not to publish papers
with contrary views, regardless of their quality.
These journals can carry a fair amount of adver-
tising, which together with wide distribution to
156 Dental Practice
the association’s membership keeps the price
moderate. In the better journals, advertising
material must pass editorial scrutiny for factual
content and taste.
A Reputable Scientific Publisher Some
journals are produced by publishers of medical
and dental texts to fill a need: Community
Dentistry and Oral Epidemiology and Journal of
Periodontal Research, published by Blackwell
Scietific Publishers, are examples. The best jour-
nals in this group are rigorously peer reviewed
and generally are the equal of those issued by
learned societies in terms of quality.
A Commercial Publisher Journals issued
by commercial publishers comprise a category
often referred to as “throwaways,” and some can
be more accurately described as magazines
rather than journals. They carry a lot of advertis-
ing, which often permits them to be distributed
free of charge, and their articles are often written
by professional in-house staff. Some do accept
contributed papers, but peer review is unusual.
The scientific quality of these journals is usually
not high, for that is not their function. These
journals fill a niche, as long as readers recognize
them for what they are.
The third step in quality determination is to
look for a listing of an editorial board, advisory
board, or consultants. These terms can be used
loosely and interchangeably, and the functions
of these groups can vary widely, from taking an
active role in journal policies to being little
more than window dressing. The presence of
such a list, however, suggests that the journal is
at least trying to keep up standards.
As the fourth step, a reader should be able to
judge the nature of the papers from a quick
perusal: research reports, case reports, opinion
pieces, reviews, political commentary. First and
most important, the reader should be able to
tell which is which. Looking over the editorials,
in those journals that carry them, can give a feel-
ing for any particular political stance the journal
may take.
The fifth step can be to scan the advertising
for the products and services presented, and the
advertising style. Better-quality journals either
have no advertising or a reasonably restrained
advertising style. Look for some statement
of advertising policy, such as is found in the
advertising index of each issue of the Journal of
the American Dental Association.
Finally, the production standards should be
checked. Typographical errors, lack of consis-
tency, and inadequate citations in references
can make a reader wonder what else is wrong
that is less readily apparent.
A professional’s ability to understand scien-
tific reports in the literature demands some
grasp of research design. Although the princi-
ples of research apply to all kinds of scientific
inquiry, the details described in the following
paragraphs relate specifically to epidemiologic
studies and to clinical trials.
CRITICAL READING—EVALUATING
THE QUALITY OF A PUBLISHED
PAPER
Hierarchy of the Quality of Information
As far as possible, knowledge upon which treat-
ment procedures and other actions are based
should come from the results of carefully struc-
tured research designs, free of bias, minimizing
random error, and carried out with human sub-
jects. This is inherently impossible in some
instances and simply lacking in others, so a
reader needs to judge the source of information
carefully when assessing the state of knowledge
on any subject. It was this need, often frustrat-
ingly unresolved, that spawned the move toward
evidence-based medicine (see Chapter 12).
The best-developed measuring scales for
assessing the quality of information in a pub-
lished report are for studies of therapeutic and
preventive products and interventions. A num-
ber of such scales have been suggested. The first
of these was developed by a Canadian panel
that had the task of appraising the value of the
routine physical examination in preventing
morbidity.2 The scale the panel constructed was
used, more or less unchanged, by the U.S.
Preventive Services Task Force a few years later
and with some modification is still being used
by that group.3 These pioneering scales can be
seen in retrospect as early steps in the growth of
evidence-based medicine. The scale in Box 11-1
gives a hierarchy for judging the quality of an
individual study that tests the value of a thera-
peutic or preventive product or intervention.
This is a broad guide, with many overlaps, but
provides a framework for judging the internal
validity of a paper, that is, the extent to which its
conclusions are supported by its methods and

results. (Note that this scale is not applicable to
judging papers on diagnosis, prognosis, appro-
priateness of policy, or economic analysis.)
Many questions regarding treatment or pre-
vention in dentistry are simply not amenable to
testing in randomized trials, either for ethical
reasons (Are amalgams harmful to human
health?) or because of inherent difficulties (Is
group practice more efficient than solo prac-
tice?). In such instances, evidence from less rig-
orous study designs must do. Case studies can
be helpful in guiding appropriate treatment,
but individual patients may be atypical, and the
treatment outcome therefore not generalizable;
that is, case studies lack external validity—they
cannot be generalized to the base population.
The opinion of an acknowledged expert is
always worth listening to, but experts are
human too and subject to bias.
In many areas of basic science, animal stud-
ies and other laboratory experiments are a
major source of information that can be applied
to humans. The fundamentals of trials involv-
ing rats, hamsters, guinea pigs, dogs, monkeys,
and other animals used in studies are the same
as those for trials with humans. The reader
should look for the special complications of
animal studies: Was the strain of rat used sus-
ceptible to the disease? Were the results poten-
tially biased by an undue number of deaths in
one group? An ever-present difficulty with ani-
mal studies is the extent to which results should
BOX 11-1 Scale for Judging the Quality of Information in Reports on Therapeutic and Preventive
Interventions in Human Studies, Ordered From Best Quality (1) to Weakest (8)2,5
1. Randomized clinical trials in humans, in which all
criteria described in Experimental Study Designs in
Chapter 13 are met.
2. Clinical trials in humans that employ concurrent
randomized controls but in which one or more
elements described in Experimental Study Designs
in Chapter 13 are missing. The more that these
elements are missing or the criteria inadequately
satisfied, the greater the threat to internal
validity.
3. Well-controlled cohort and case-control studies, or
clinical trials without random allocation, or field trials
(in which the community, rather than the individual,
is the unit of study).
11 Reading the Dental Literature 157
be applied to humans. The same concern
applies to all laboratory procedures: Does the
dental enamel in the test tube react the same
way as it does in the mouth? Are the bacteria
produced from pure culture the same as those
found in the oral environment? The ideal occur-
rence for reaching conclusions is when the
results of laboratory studies are confirmed in
humans, but again this happy circumstance
often is not possible.
Criteria for Judging the Quality
of an Individual Paper
There are essentially four kinds of papers pub-
lished in journals. These can be categorized as
follows:
Research Reports, which describe original
clinical, basic, or epidemiologic research. A
question is identified, a study is designed to test
the question, the results are discussed, and
some conclusions are reached.
Case Reports, which are accounts by clini-
cians of unusual manifestations of disease
conditions, treatment outcomes, or disease pro-
gression. In many areas of surgery, randomized
trials will never be carried out because of the
inherent difficulties, so case reports form the
body of literature on many surgical procedures.
Reviews of the literature, which summarize
knowledge in a particular area (the narrative
review is referred to here; systematic reviews are
discussed in Chapter 12). A narrative review is a
4. Clinical trials without concurrent control groups,
such as those using historical controls, and
retrospective cohort studies. The better examples
here can be considered equal to those in item 3.
5. Cross-sectional studies without controls, in which a
group’s oral health status is matched against some
past exposure to suspected disease-causing or
disease-preventing agents.
6. Descriptive surveys, in which present oral health is
surveyed and there is informed speculation as to the
influences that led to the observed status.
7. Case reports.
8. Personal opinion, subjective impressions, and
anecdotal accounts.
158 Dental Practice
traditional approach in which a knowledgeable
person or persons collects the published infor-
mation on a subject and reaches conclusions on
what the literature collectively says about the
issue in question. The best narrative reviews are
superb additions to the literature; the poorest
ones, narrow and biased. This type of review is
frequently presented at a conference or sympo-
sium, and when such reviews are done well they
can be among the most influential and valuable
works in the literature.
Commentaries, in which some documented
facts are used as a basis for urging program
development, health policy, or some other kind
of action. Commentaries can vary greatly in
quality, ranging from beautiful insights to
hopelessly biased diatribes.
The essential features to look for when read-
ing a paper in the literature can be presented in
semichecklist form, and this is done for three
types of reports in Boxes 11-2 to 11-4 (case
reports do not fit this model). The list may seem
rather long at first, but with practice readers will
soon be able to apply these criteria quickly and
in due course almost unconsciously. The goal,
in fact, is that their application become an auto-
matic feature of reading reports in journals.
As evidence-based medicine developed, it
quickly became apparent that a major stum-
bling block to synthesizing clinical trial reports
from the literature was their lack of homo-
geneity. Vital information (e.g., method of
subject allocation, control of exposure, data
reliability) was often presented in vague
terms or, worse, not mentioned at all. The
response to this problem was the development
of a protocol known as the CONSORT
Statement (CONSORT is an acronym for
Consolidated Standards of Reporting Trials),
which journals are urged to adopt as a means of
ensuring that all published clinical trials con-
tain adequate detail on the methods used. The
goal is to achieve homogeneity in reporting,
which in turn permits meta-analysis (see
Chapter 12) and improves the quality of sys-
tematic reviews.4 When authors adhere to
CONSORT standards their papers are easier to
read, and it is also easier for readers to judge the
quality of the papers. Protocols for reporting
other kinds of scientific study have been devel-
oped in the wake of CONSORT; these are dis-
cussed in Chapter 12.
There are a few other aspects common to all
reports in the literature. Reports should have a
concise yet informative title that allows the
reader to recognize the content and assists in
electronic retrieval. A good abstract permits
readers to identify quickly the basic contents of
the paper. An abstract for a research paper
should (1) state the objectives and scope of the
investigation, (2) describe briefly the methods
used, (3) summarize the findings, and (4) state
the main conclusions. Some journals require
that an abstract be written strictly to that format.
The wise author chooses words for the abstract
that are similar to the MeSH (Medical Subject
Headings) terms under which the paper will be
indexed. Headings specific to dentistry are espe-
cially helpful because these are underrepre-
sented in MEDLINE (Medical Literature,
Analysis, and Retrieval System Online, described
in the next section). Abstracts should never con-
tain information or conclusions not stated in
the body of the report. Brevity (no more than
250 words helps electronic storage and retrieval)
requires that abstracts be objective, straightfor-
ward, and free of opinion or speculation.
FINDING THE REPORTS YOU NEED
IN THE LITERATURE
Practitioners often need to find information
about a given subject: What is this material that
a supply house salesman is pushing? Do
sealants work on primary teeth? Has this new
cavity liner been adequately tested? The list is
endless. Dental professionals need to know
how to search the vast literature efficiently to
find the information they need to reach a con-
clusion. Fortunately, the rapidly developing
electronic methods for searching the literature
make this task much less arduous than it once
was.
A useful start is the reference lists at the ends
of textbook chapters, although the earlier
caveats on obsolete material in textbooks per-
tains to the references too. Not only do they risk
being dated, but such reference lists often are
not complete, or they can reflect an author’s
bias or incomplete grasp of a subject. These ref-
erence lists can be a good starting place,
although usually more is needed. Good reviews
of the literature on a related topic can be useful.
Although the conclusions of the review may be

BOX 11-2 Quality Issues in Judging Research Reports
General Issues
●
Nature of the journal in which the report appeared (see
discussion on journals in the text).
●
Qualifications of the authors. Is at least one a well-
known researcher? Is there evidence of research
training among the authors? Are they affiliated with a
reputable institution?
●
Research funding. If the work was commercially
funded, is there any reason to believe that the
sponsors might have influenced the results?
●
Date of publication. Knowledge is moving rapidly in
some fields, less so in others. Is the report likely to
have been superseded by more recent work?
Research Specifics
●
Is the research question, purpose of the paper, and a
hypothesis clear and succinctly stated? If not, is a
hypothesis at least implied?
●
Although the review of current knowledge must often
be brief in a research report, is it a balanced summary
of previous work? (The “selective” review to support a
particular point of view is unfortunately not unknown.)
●
Are the measurement variables and other terms
specifically defined? If standard terms and measures
are being used, are references given for their
definition? If new measures are being introduced, are
they clearly defined and is it made clear why existing
ones cannot be used? (These questions are all aimed
at checking internal validity.)
●
If the study involves humans, is the population
studied appropriate in view of the stated purposes?
Does the report give details on participants in the
study: the numbers of people approached, those who
agreed to begin the study, and those who remained at
the end?
enough for some purposes, the reader will often
want to follow up on some of the papers cited
in the review.
The main repository of bibliographic infor-
mation on the biomedical literature is the Index
Medicus, a vast compendium managed by the
National Library of Medicine (NLM), located on
the campus of the National Institutes of Health
in Bethesda, Maryland. A bibliographic guide to
the dental literature for years was to be found in
the bound copies of the Index to Dental
Literature, although NLM stopped production of
11 Reading the Dental Literature 159
●
Is the research design appropriate to test the
hypothesis and thus answer the underlying question?
●
Are the materials and methods clearly detailed? Are
measurements applied as described? Have the
researchers taken steps to ensure that the measures
are being recorded as reliably as possible? With
regard to this latter point, if there are several
examiners in an epidemiologic study, are they
experienced in such research or have they been
trained and their evaluations calibrated for this
project? Are any checks made to ensure examiner
reliability?
●
Is the statistical analysis appropriate for the types of
data collected? Have the authors presented sufficient
data in the way of tables or graphics to permit the
reader to check this question? Are the statistical tests
used appropriate for testing the stated hypothesis?
●
Does the discussion look critically at any limitations of
the methods used? Are appropriate comparisons
made with previous work and reasons discerned for
similarities or differences? Is a fair assessment of the
relevance of the work made, with some specifics given
for the next steps?
●
Are the conclusions clear and warranted by the results
of the research? Have the authors made suitable
distinction between statistical significance and clinical
importance?
●
Is the paper clearly and concisely written? Does the
abstract give a clear profile of the study?
●
Have the issues of informed consent and ethical
research been dealt with adequately and clearly
stated?
●
If the report is a clinical trial, have the reporting
requirements listed in the CONSORT (Consolidated
Standards of Reporting Trials) Statement been met?
the printed Index in the late 1990s. Searching
the biomedical literature today is a computer-
ized operation, involving a search of electronic
databases and the World Wide Web. All bio-
medical literature since 1966 indexed by the
NLM is now searchable on-line through MED-
LINE, biomedicine’s primary database, though
by no means the only one in which dental prac-
titioners will be interested. MEDLINE indexes
most, but not all, of the world’s biomedical
research literature, although EMBASE, another
biomedical database, is stronger in non-English
160 Dental Practice
BOX 11-3 Quality Issues in Judging Narrative Reviews of the Literature
●
Is the subject of the review clearly stated and are its
boundaries delineated?
●
As far as you can determine, is all appropriate work
included in the review?
●
Is there a fair but critical analysis of the reports
reviewed, or does the author(s) seem to be
emphasizing only one side of an issue?
BOX 11-4 Quality Issues in Judging Commentaries
●
Has the author used whatever factual basis is available
to develop the case? (Hard data should always be
used as much as possible, even though some
conclusions must be reached with less information
than is desirable.)
publications and the drug literature. The most
popular version of MEDLINE is PubMed,
designed for quick and easy use by the busy
practitioner. The Clinical Queries option in
PubMed allows the clinician to quickly focus a
large search on the question of interest.
Practitioners anywhere in the world need only a
personal computer, appropriate web browser
software, and a connection (preferably high-
speed) to the World Wide Web (of course, this
service also needs to be paid for). A number of
commercial services carry MEDLINE and
related databases, and the search process is
becoming more and more user friendly.
When one first begins to use MEDLINE, the
effect can be overwhelming: a tidal wave of
information gushes over the user, often far more
than can be readily digested. Sometimes this
reflects reality; there is just so much more pub-
lished on an issue than the user may have imag-
ined. At other times it means that the search is
too broad and that a lot of inappropriate mate-
rial is included. Practice in the use of keywords
and increasing familiarity with the MeSH termi-
nology make searching much more efficient. It
does not take long for even a technophobe to
conduct an efficient search. A dental practi-
tioner with a computer in the back room of the
practice can easily search an issue over a
lunchtime sandwich and refine the search to a
●
Does the review critically assess the value of different
research reports, or are they all taken at face value and
given equal merit? Lack of critical assessment
weakens a review.
●
Is there respect for various points of view?
●
Are conclusions warranted by the argument made, or
is there a sense of preconceived conclusions?
usable number of relevant references. Abstracts
now accompany the reference citation for
most journals, which makes the search even
more efficient, and full-text paging is becoming
more common. This means that the full article
is available from the web for an increasing
number of biomedical journals. On-line sub-
scriptions can be purchased in the same way as
are regular subscriptions; indeed, many see on-
line subscriptions as the future of the scientific
literature.
The result of a search is a stream of refer-
ences, most with abstracts, that flow across the
screen; unless they are captured and stored, the
search is a transitory thing. Therefore, to go
along with the electronic searching procedures,
bibliographic database software permits down-
loading of the search results into the storage
database. The search is performed, the desired
references are selected from among those
perused, and these are downloaded into the
database; then they are on hand permanently.
Once we get accustomed to this way of search-
ing the literature, it is difficult to know how we
ever got along without it.
The amount of useful information on the
World Wide Web is growing at a staggering rate.
It is assumed that readers are familiar with the
web to some extent. For those who are not, the
World Wide Web is a means of storing text,

graphics, and audio material in a computer
server in such a way that anyone in the world
with web-browsing software can retrieve it.
Although the web generally remains a delight-
fully anarchic affair, a lot of useful information
can be found there. An example was given in
Chapter 3, which noted that the ADA’s
Principles of Ethics are now accessed through
the ADA home page on the web rather than
published in print. A vast amount of health-
related information can be found on the web-
sites for the ADA, National Institutes of Health,
Centers for Disease Control and Prevention,
and World Health Organization. Also available
now is an encyclopedic guide to searching and
finding information on the web, available both
as a traditional book (three volumes) and on
CD-ROM.1
The only snag in these developments is that
information located in the search still has to
be read! Photocopying is getting easier and
cheaper, and dental school librarians will
obtain a needed journal from interlibrary loan
if necessary. Whether or not they have access to
a dental school library, health practitioners can
submit on-line requests for interlibrary loans
from anywhere in the country using PubMed’s
Loansome Doc system. Even photocopying from
a journal may become largely obsolete as full-
text electronic storage grows. When full-text
storage develops completely, practitioners in
11 Reading the Dental Literature 161
the most remote geographic locations will need
only a computer and an Internet connection to
have the entire dental literature at their finger-
tips, literally! The technology for all this is in
existence now, and future developments will
depend on sorting out the legal and economic
ramifications. We can be virtually certain that
progress in the area of keeping up with the liter-
ature will continue to be rapid and that scien-
tific knowledge will continue to become more
readily available all the time.
REFERENCES
1. Anderson PL, Allee NJ. Medical Library Association ency-
clopedic guide to searching and finding health informa-
tion on the web. New York: Medical Library Association
and Neal-Schuman Publishers, 2004, website: http://
www-personal.umich.edu/~pfa/mlaguide/indextest.
html. Accessed April 3, 2004.
2. Canadian Task Force on the Periodic Health
Examination. The periodic health examination. J Can
Med Assoc 1979;121:1193–1254.
3. Harris RP, Helfand M, Woolf SH, et al. Current methods
of the US Preventive Services Task Force; a review of the
process. Am J Prev Med 2002;20(3 Suppl):21–35.
4. Moher D, Schultz KF, Altman DG, for the CONSORT
group. Revised recommendations for improving
the quality of reports of parallel group randomized
trials 2001, website: http://www.consort-statement.org/
revisedstatement.htm#app. Accessed November 28,
2003.
5. US Preventive Services Task Force. Guide to clinical pre-
ventive services. 2nd ed. Washington DC: US
Department of Health and Human Services, 1996.
 12 Evidence-Based Dentistry
WHAT IS EVIDENCE-BASED DENTISTRY?
THE ART AND SCIENCE OF DENTISTRY
RATING THE QUALITY OF THE LITERATURE
THE SYSTEMATIC REVIEW
Conducting a Systematic Review
EXAMPLES OF EVIDENCE-BASED DENTISTRY
Are Powered Toothbrushes Superior to Manual
Cleaning for Oral Health?
What do you do when a periodontal patient
says, “I read in a magazine that gum disease can
cause a heart attack but that there is a drug avail-
able to prevent this. Should I be taking this
drug?” Chances are that you don’t know how to
respond. You may have studied the relationship
between periodontitis and cardiovascular dis-
ease (see Chapters 21 and 29), but you have
never heard of the drug the patient describes.
Your first instinct is probably to dismiss the
whole thing, but you have a nagging feeling that
perhaps there is something in it. So what do you
do? That is the theme of this chapter: to look at
the emerging field of evidence-based dentistry
(EBD) and to see how you can use it in practice.
This chapter describes what EBD is, why
increased attention is being given to EBD, how
this emphasis will affect oral health profession-
als in the future, and what responsibilities come
with adherence to evidence-based practice.
WHAT IS EVIDENCE-BASED
DENTISTRY?
EBD is sometimes described as doing the right
thing, for the right patient, at the right time.
This definition is succinct and hard to dispute,
but it still leaves the practitioner with little con-
crete direction in the day-to-day, patient-by-
patient decisions that must be made in practice.
What, in fact, is the right thing to do in each sit-
162
What Are the Success Rates of Different
Implant Systems?
RESPONSIBILITIES OF PRACTITIONERS
CURRENT STATE OF THE SCIENCE
LIMITATIONS OF EVIDENCE-BASED
DENTISTRY
uation that presents itself, who is the right
patient to treat with which procedure, and
when is the time right? These are complex ques-
tions and usually do not have clear-cut answers.
A more detailed definition of evidence-based
medicine (EBM), from which EBD is derived, is
the following:
The conscientious, explicit and judicious use of current
best evidence in making decisions about the care of individ-
ual patients. The practice of evidence-based medicine
means integrating individual clinical expertise with the best
available external clinical evidence from systematic
research.21
There are three essential components of
EBM: the scientific base for any treatment deci-
sion a practitioner makes, the clinical expertise
of the practitioner, and the patient’s values.
Dentistry has come to this field later than medi-
cine and has for the most part adopted the same
language and conventions. So the definition
just given for EBM is applied to EBD, as are the
three components, although this more detailed
definition also requires interpretation before
the clinician can be confident about how it
applies in the day-to-day clinical practice of
dentistry. Both EBM and EBD relate to patient
care (rather than research or administration)
and are invoked when the practitioner is seek-
ing to make the best treatment decision for a
particular patient.

But hasn’t dentistry always based treatment
decisions on scientific evidence? Well, yes and
no, as we’ll discuss further. The landmark Gies
report of 1926 noted “the growth of quackery”
during the nineteenth century,9 and even the
1995 Institute of Medicine report on the future
of dental education recommended greater
development of the scientific base in dental
practice.11 The modern evidence-based approach
in medicine, which got underway during the
1970s, is now well established, one could
almost say institutionalized. The years between
the 1970s and the present day saw an evolution
of the methods for the systematic collection of
information in EBM and its application to clini-
cal practice, so that today, as we develop EBD,
we can benefit from the experience of our med-
ical colleagues. What is now emerging in den-
tistry is the formal recognition that clinical
decision making requires the application of the
rigorous rules of evidence. One sign of this
increased attention is the establishment of two
journals on the topic: Evidence-Based Dentistry
first appeared as a supplement to the British
Dental Journal in 1998 and became a stand-
alone journal in 2000. The Journal of Evidence-
Based Dental Practice began publication in the
United States in 2001.
THE ART AND SCIENCE
OF DENTISTRY
The phrase the art and science of dentistry means
that when we care for our patients we combine
our clinical acumen, experience, and human
sensitivity with procedures that are based on the
most up-to-date science. Essentially, the “art” of
dentistry is the acceptance of the individuality
of each patient. We recognize that a treatment
we think appropriate for one person will not
necessarily be appropriate for another with the
same condition. We use the art side of our prac-
tice to assess the patient’s interest in his or her
oral health when formulating a treatment plan.
We also factor into the treatment plan the
patient’s age, existing state of oral and general
health, and ability and willingness to pay for
treatment. The art of dentistry also includes the
clinician’s individual ability in using certain
materials or techniques. Sometimes a clinician
will have a special knack for working with a
material or procedure and so can make a given
12 Evidence-Based Dentistry 163
treatment perform better than the average clini-
cian would.
This art aspect of clinical dentistry should
remain. It is only out of place when the opin-
ions, beliefs, and attitudes of the dentist, no
matter how well intentioned, are allowed to
override facts that are clearly demonstrated
through science. There should be a mix of art
and science in each treatment plan, but the pro-
cedures that we consider as treatment options
should, as far as possible, be justified by science.
There will be occasions in which a scientific
base for a treatment option is nonexistent, and
in these cases the practitioner has to determine
what the best practices are. In such cases it is up
to the dental research community to see that
resources are directed into these areas to ensure
that the necessary scientific base is developed.
It is useful to distinguish between the princi-
ples of EBD and the methods that have been
proposed for implementing it. Regarding the
principles there is little dispute, for no one can
argue against using evidence as the basis for
care. This philosophical stance, however, is
immediately followed by the practical issues of
(1) what qualifies as evidence, and (2) how we
evaluate that evidence. With EBD, the tradi-
tional ad hoc and subjective approach to these
issues is replaced by explicit and objective
methods to evaluate the available evidence. We
recognize that today it is more difficult than
ever for clinicians to assess all of the rapidly
expanding treatment options before deciding
on their value to their patients. Although the
methods of EBD are not a panacea for the chal-
lenge of increased options, they do provide a
framework for a systematic and unbiased
approach to evaluating those options. Rather
than requiring an ad hoc assessment by each
individual clinician to determine the strength of
the scientific evidence on each aspect of dental
care, EBD uses a systematic process to assemble,
evaluate, and summarize the evidence on par-
ticular treatment questions.
RATING THE QUALITY
OF THE LITERATURE
If the quality of the scientific evidence is to form
an important part of our clinical decision mak-
ing, then how do we judge the quality of that
evidence? In Chapter 11, we looked at how to
164 Dental Practice

Table 12-1 Scale for categorizing the strength of evidence for a program or procedure4
Code Criteria

I Evidence obtained from one or more properly conducted randomized clinical trials (i.e., one using
concurrent controls, double-blind design, placebo, valid and reliable measurements, and well-
controlled study protocols).
II-1 Evidence obtained from one or more controlled clinical trials without randomization (i.e., one using
systematic subject selection, some type of concurrent controls, valid and reliable measurements, and
well-controlled study protocols).
II-2 Evidence obtained from one or more well-designed cohort or case-control analytic studies, preferably
from more than one center or research group.
II-3 Evidence obtained from cross-sectional comparisons involving subjects at different times and places, or
studies with historical controls. Dramatic results in uncontrolled experiments (such as the results of the
introduction of penicillin treatment in the 1940s) could also be regarded as this type of evidence.
III Opinions of respected authorities, based on clinical experience; descriptive studies or case reports; or
reports of expert committees.

evaluate the quality of an individual paper. In
terms of assembling components of the scien-
tific base to support a treatment procedure,
EBM and EBD extend that analysis by objec-
tively measuring the quantity and quality of the
body of evidence on a subject. The traditional
process is by means of the narrative review (see
Chapter 11) in which an expert, or experts,
assesses the literature on the subject and then
reaches conclusions. Again as noted in Chapter
11, the quality of such reviews varies from bril-
liant to mediocre or even misleading. This range
results from differences in the research atten-
tion the subject has received, the thoroughness
of the literature search, and the ability and
objectivity of the reviewer.
An inherent problem in any literature review
is the variation in quality of research reports on
the subject. As stated in Chapter 11, to be of
value any review must be a critical review;
that is, the variation in quality of the various
research reports must be explicitly recognized.
Recognition is a good first step, but the reviewer
still has to deal with the issue. This variation in
the quality of the literature was a problem fac-
ing a Canadian expert panel in the 1970s whose
task was to assess the value of the annual physi-
cal examination in preventing mortality and
morbidity.4 To deal with the range in quality of
the papers on the subject, the Canadian group
developed a hierarchical scale to give a quality
score to each paper the members were reading.
This scale is shown in Table 12-1. These quality
scores were the basis for the recommendations
issued on the use or rejection of the procedure
(Table 12-2). This methodologic approach had
sufficient appeal to be adopted a few years later
by the U.S. Preventive Services Task Force25 and,
in slightly modified form, by the Centers for
Disease Control and Prevention for a major
report on fluoride (see Chapter 26) a few years
later.26 This approach does require some sum-
mary judgments by the review panel when the
research reports on testing of a procedure are of
mixed quality. Scaling the quality of a whole
body of evidence as a unit still has some appli-
cation, although the principal method now
used for assessing the quality of a body of evi-
dence is the systematic review, which is based on
grading each of the individual reports selected
and then reaching an overall conclusion.
THE SYSTEMATIC REVIEW
For most of us, the most convenient way to catch
up on a subject is to read reviews of the litera-
ture. The traditional format is the narrative
review, which often takes the form of a paper
given at a conference or symposium, in which
the authors assess the information from
published reports on a topic and then reach a
conclusion based on the weight of evidence.
Narrative reviews have been around for ages and
generally have served a valuable purpose, but
they can have limitations because of their sub-
jective nature.18 The first problem with any type
of review is that not all research gets published.
A significant number of clinical trials, in particu-
lar, do not find their way into our journals.5
Corporate sponsors are generally reluctant to
 12 Evidence-Based Dentistry 165

Table 12-2 Scale for strength of recommendation on the use or rejection of a procedure.4
Grade Criterion

A There is good evidence to support the use of the procedure.

B There is fair evidence to support the use of the procedure.
C There is a lack of evidence to enable a specific recommendation to be made; i.e., the subject has not been
adequately tested. This grade will also apply to mixed evidence; i.e., some studies support the use of
the procedure and some oppose it.
D There is fair evidence to reject the use of the procedure.
E There is good evidence to reject the use of the procedure.

publish clinical trials with so-called negative
results,6 meaning that a benefit from the tested
product or procedure could not be demon-
strated, and accordingly researchers tend not to
submit reports with negative results.19 This par-
ticular problem is called publication bias. Another
aspect of publication bias is the fact that only
two thirds of published abstracts, which cannot
provide methodologic detail, get into print as
full publications within a 2-year period.22
So, what can be done about this? The response
to these problems of bias and incomplete infor-
mation in narrative reviews is the systematic
review, which reduces the potential for bias at all
levels. A systematic review is defined as one in
which there is a comprehensive search for all rele-
vant studies on a specific topic and those identi-
fied are then appraised and synthesized according
to predetermined and explicit criteria.13
There is a philosophical link between a sys-
tematic review and a scientific study. Just as a
good report of an experiment carried out in the
laboratory gives sufficient methodologic detail
to let the reader know just how the results were
achieved, the existence of written protocols in a
systematic review lets the reader know just how
the authors came to the conclusions they did.
The word is transparency. Systematic reviews are
transparent in that the reader is given all the
details of the search strategy, inclusion and
exclusion criteria, quality ratings, and the way
final conclusions were reached. This is rarely the
case with a narrative review, for which the
reader usually must just trust the authors. In a
systematic review, the reader knows exactly how
the authors arrived at their conclusions.
The systematic review was developed for
judging the efficacy of preventive or therapeutic
procedures and hence is best geared to assess the
quality of randomized clinical trials (RCTs). It
quickly became evident that judging the quality
of an RCT could be frustrated when the original
report was deficient in some essential details
(e.g., group allocation procedures, control of the
procedure, statistical methods). This issue is sep-
arate from the quality of the study itself—the
study may or may not be of top quality, but the
report is deficient. This problem led a group of
concerned researchers and editors to develop
criteria for what should be included in the report
of an RCT so that the quality of the study could
be determined. The result was a checklist known
as the CONSORT Statement.15 CONSORT is
an acronym for Consolidated Standards of
Reporting Trials. The more journals that sub-
scribe to CONSORT principles, the more readily
comparable RCT reports will become, and the
more precise systematic reviews will become.
The idea of standards to promote more uni-
form reporting has now spread to encompass
other types of research manuscripts. For meta-
analyses, in which a number of RCTs are
combined to increase statistical power, there
is QUORUM (Quality of Reporting Meta-
Analyses)15 and for papers studying diagnostic
accuracy there is STARD (Standards for Reporting
of Diagnostic Accuracy).3 The other member of
this menagerie is MOOSE (Meta-Analyses of
Observational Studies in Epidemiology), which
specifies reporting standards for observational
studies, the designs of which cover a broader
spectrum than do those of RCTs.23
Conducting A Systematic Review
Because the systematic review is the cornerstone
of EBD, some detail are given on how a systematic
review is put together. Just as with a research pro-
posal, all the protocols are written down before
the search begins: making up the rules or acting
on whims as one goes along is not allowed.
166 Dental Practice
Question to Be Examined
The purpose of a narrative review is usually
rather general, for example, to assess the effect
of oral hygiene on the prevention of gingivitis.
In a systematic review, the question is sharp-
ened, just as in a research proposal a broad
research question is honed into a hypothesis
that can be tested experimentally. The oral
hygiene and gingivitis question for systematic
review would then become, for example, “Does
toothbrushing once every 48 hours prevent gin-
givitis?” Or the time interval selected might be
24 hours, which could result in the inclusion of
some different studies in the review and might
lead to a different conclusion. Or the question
could substitute dental flossing for toothbrush-
ing, which again would change the direction of
the search. The question to be examined in a
systematic review must be stated precisely and
explicitly.
Inclusion and Exclusion Criteria
The inclusion and exclusion criteria follow from
the question, and the criteria must be stated so
the reader can be satisfied that there is little
chance of inclusion bias, that is, that not all pub-
lications were considered or that inappropriate
ones were included. To illustrate, one such crite-
rion is language of publication. Americans tend
to read only the English-language literature, but
in some fields this can be a clear source of inclu-
sion bias.16 Another criterion is the range of the
outcome. If the subject is the effect of fluoride
varnish in preventing caries, for example, the
reviewers must specify whether they intend to
include root caries as well as coronal caries,
caries in the primary as well as the permanent
dentition, noncavitated lesions as well as cavi-
ties, secondary caries, and so on. Age of people
studied must also be considered.
Search Strategy
Electronic searching is the logical starting point,
and the reader needs to know which databases
were searched. MEDLINE (Medical Literature,
Analysis, and Retrieval System Online) is the
principal database for reports in dentistry, but
only about half the papers on most topics can
be found readily in MEDLINE, mainly because
of inappropriate indexing.7 It may also take up
to a year for recent papers to be indexed in
MEDLINE. This is not a criticism of MEDLINE,
for relevant reports are usually in the MEDLINE
database somewhere, but if they are inappropri-
ately indexed they will not be found with the
usual keywords. Other databases can profitably
be added to the search for many fields of study.
The reviewers also must state the keywords used
in the search,12 again to make the search
method as transparent as possible.
Electronic searching usually needs to be aug-
mented by hand searching, largely because of
the chances of missing improperly indexed
reports in MEDLINE and other databases, as
mentioned earlier. Hand searching is what we
used to do all the time before there were elec-
tronic databases. It consists of going through
the references listed at the ends of some publi-
cations and going through back copies of spe-
cific journals in which publications on the topic
are most likely to have appeared. Hand search-
ing is tedious and time consuming, but it is
absolutely necessary if inclusion bias is to be
avoided.
Criteria for Study Quality
The step of developing criteria for study quality
sets the attributes that a report must possess to
be included in the final analysis. For example,
with RCTs the reviewer wants a description of
how subjects were allocated to groups. If the use
of random allocation as an inclusion criterion
results in the discarding of virtually all the stud-
ies because no trials used random allocation,
then a less rigorous criterion would probably
have to be written. Because one of the results of
systematic reviews is identification of further
research needs, in this instance a recommenda-
tion for true RCTs might be a logical conclusion.
Development of Conclusions
Assessment of the final group of reports can be
qualitative or quantitative. Qualitative means
that no further statistical analysis is done by the
reviewer; instead, the studies are grouped as
being on one side of the question or another,
and a final conclusion is then reached, based on
where most results lie. Further quantitative
analysis can in some circumstances be carried
out by combining the data from a number of
studies to produce a single estimate of effect, a
process called meta-analysis.13 The rationale for
meta-analysis is that the statistical power of the
estimate can be increased by enlarging the

sample size. The limitation to this procedure is
that there must be design homogeneity among
the studies to be combined; otherwise, the exer-
cise loses validity.
EXAMPLES OF EVIDENCE-BASED
DENTISTRY
Now that formal EBD approaches to evaluating
the research literature have been developed,
there is a rapidly growing body of such reviews.
Many can be found in the Cochrane Library
(http://www.update-software.com/cochrane/
abstract.htm), an on-line catalog of systematic
reviews to augment the published journals (Box
12-1). Two such reviews are outlined here as
examples of how these reviews can help the cli-
nician provide authoritative scientifically based
information and treatment choices to patients.
BOX 12-1 The Cochrane Collaboration
The Cochrane Collaboration, launched in 1993 and named
after the late British epidemiologist Archie Cochrane, is an
international nonprofit organization whose mission is to
make up-to-date information about the effects of health care
readily available to clinicians. It was born from Cochrane’s
frequent observations that, although many clinical trials had
been carried out in medicine, there was no systematic
collection of these trials that a busy practitioner could
consult. The main product of the Cochrane Collaboration is
the Cochrane Database of Systematic Reviews, which
forms part of the Cochrane Library.24 The Cochrane Library
is an electronic resource that by 2004 contained some 2000
regularly updated systematic reviews and other sources of
information. There are 51 Cochrane review groups around
the world, each focusing on a specific disease or group of
problems, including an oral health group
(http://www.cochrane-oral.man.ac.uk/) through which a
number of systematic reviews have already been archived.
There are a number of funding sources for the Cochrane
Collaboration, but its acceptance around the world in such a
short time is largely due to volunteer effort.
Much of this success is a result of the rigorous
standards that the Collaboration maintains at all levels
(http://www.cochrane.dk/cochrane/handbook/hbook.
htm). Anyone wishing to carry out a systematic review
for the Cochrane Library must first register a title with a
Cochrane review group, have the title accepted, and
then submit a protocol for the systematic review. The
12 Evidence-Based Dentistry 167
EBD Example: Are Powered Toothbrushes
Superior to Manual Cleaning for
Oral Health?
With the proliferation of powered toothbrushes
that are marketed directly to the consumer, den-
tists are asked about them by patients. The
analysis27 of a Cochrane review10 compares
plaque removal and gingivitis in people using
manual toothbrushes and in those using one of
six different types of powered toothbrushes. An
early problem was that most of the studies in
the literature were excluded from the review
because of various shortcomings in their design,
execution, or reporting. This immediately
points up to the reader the importance of not
being unduly influenced by individual litera-
ture reports that do not meet contemporary
standards for quality research and reporting.
protocol is then sent out for internal and external peer
review. Protocols, like papers submitted to a journal,
can at this stage be accepted, rejected, or revised.
Protocols for which the final review has not been
completed are listed, so readers can see what reviews
are coming up. The same rigorous refereeing process is
carried out when the systematic review is completed.
A particular feature of the Cochrane system is that
reviews are not intended to be carved in stone and left
there. Quite the opposite in fact, for it is intended that
reviews be updated periodically as new information
comes out. Because the protocols and procedural
methods are published as an integral part of the review,
updating can be carried out by the original author(s) or
by someone else. Readers can then be assured that
what they read in a Cochrane review represents the
most up-to-date summation there is.
There is already an impressive list of completed
Cochrane reviews. Although access to the full reviews in
the Cochrane Library usually requires a subscription,
detailed abstracts of the Cochrane reviews are available
on-line without charge (http://www.cochrane.org/
cochrane/revabstr/ORALAbstractIndex.htm) and are
beginning to appear in other publications.
Access to the Cochrane Library is free of charge in
many countries. Further details can be found at
http://www.update-software.com/cochrane/
provisions.htm.
168 Dental Practice
After carefully proceeding through the state-
ment of the question, inclusion and exclusion
criteria, the search strategy, and the criteria for
judging quality, this systematic review reported
the following primary findings:
●
For powered toothbrushes with oscillation-
rotation action, plaque and gingivitis
scores were 7%-17% lower than for manual
toothbrushes.
●
The studies were of insufficient duration to
determine whether these reductions are rel-
evant to the development of destructive
periodontal disease.
●
An insufficient number of high-quality
studies were available to judge whether
other types of powered toothbrushes were
superior to manual toothbrushes.
●
There was no evidence that powered tooth-
brushes were more likely to cause injury
than manual toothbrushes.
●
No information on durability, reliability,
and cost of powered toothbrushes was pro-
vided by the available studies.
With this kind of information, the clinician
is able to provide authoritative information to
patients and can be confident that the informa-
tion provided is realistic and does not promise
more than can be supported by the best-quality
research available.
EBD Example: What Are the Success
Rates of Different Implant Systems?
Estimates were that in the year 2000 there were
nearly 1300 different implant configurations
available, and manufacturers are rapidly placing
new systems on the market while just as rapidly
removing older ones.2 The clinician is thus
swamped with a bewildering array of choices
when trying to make the best selection to rec-
ommend to a patient. The systematic review on
implant success rates provides the clinician with
some assurance in selecting from this otherwise
very confusing morass.8,28 Within the limita-
tions imposed by the rapid turnover of available
implant types and by the fact that only five
high-quality RCTs were identified, the primary
conclusions reached by the reviewers were the
following:
●
There was no difference in apparent suc-
cess, up to 3 years after placement, among
the implant systems of the six manufactur-
ers whose systems were studied.
●
During the follow-up periods of 1-3 years,
only 25 of 957 implants were judged to
have failed. This indicates a high success
rate, at least in the short term.
The reviewers noted that, in the case of
implants, the results of RCTs may provide only
part of the story about the level of success that a
clinician might expect. The level of care given to
patient selection in an RCT, and the level of
experience of the clinicians involved, may differ
from that in the average clinical practice, and
these factors probably contributed to the likeli-
hood of success.
RESPONSIBILITIES OF
PRACTITIONERS
Individual dental practitioners are not expected
to conduct systematic reviews on their own for
each clinical question that they encounter.
Conducting systematic reviews efficiently and
effectively requires extensive training and prac-
tice, well beyond what can be reasonably
expected from all clinicians. The responsibility
for most clinicians is thus to be aware of, and to
use wherever applicable, the findings from sys-
temic reviews carried out by others. If the process
were to stop when a review was completed, and
the review were simply to gather dust on the
library shelf, it would provide little benefit in
improving oral health care. What obviously must
follow the systematic review is a process to put
the results into practice. Indeed, EBD explicitly
incorporates both a research component (along
with the systematic review) and the translation of
that research into practice.1
Dental and dental hygiene education has at
least two primary tasks. The first is to teach stu-
dents what are the best available procedures
and how to perform them competently, a
process demanding an emphasis on manual
skills. The second is to instill in students the
recognition, indeed the certainty, that much of
what they are learning will become obsolete
during their lives in practice. The challenge for
the busy clinician is to recognize when this has
occurred, yet neither to replace the outmoded
treatment with the latest inadequately tested
fad nor to wait too long so that patients are
receiving outdated care.
At the very least, the concept of EBD should
make it routine for the clinician to consider all

options when treating each patient, rather than
relying on comfortable habits and familiar pro-
cedures. The clinician must routinely ask,
“Could I have misdiagnosed this condition?”
and “What are the possible alternative diag-
noses?” When preventive and restorative
choices are made, the clinician must ask, “What
is the state of knowledge concerning this proce-
dure or material?” and “What is the likelihood
that this patient will benefit from this proce-
dure?” Also, “What are the possible risks associ-
ated with this procedure and is the probability
of success sufficient to tolerate those risks?”
Furthermore, “How does the balance among
these considerations fit with the preferences
of the patient and the costs involved?” Although
the process may at first seem cumbersome
and involved, with routine use it will become
second nature. Moreover, it is part of the funda-
mental responsibility of a health care profes-
sional to assure that the best possible care is
being provided to each patient. At the very least,
EBD has made us aware of the continuing
responsibility of every practitioner to be as up
to date as possible in knowledge of the scientific
literature. It further has shown us that simply
providing the same service or set of services to
virtually every patient is unlikely to be consis-
tent with providing the best possible care.
The concepts of EBD also make it clear that
the challenge for the clinician is never ending.
The right thing, the right patient, and the right
time will constantly evolve as change inex-
orably takes place in disease patterns, our
understanding of oral diseases and conditions,
the available therapies and materials, and
patient preferences.
CURRENT STATE OF THE SCIENCE
It will be a long and slow process to conduct
the necessary RCTs and then to mount the sys-
tematic reviews to cover even a small proportion
of all of the necessary details of modern den-
tal practice. Even in some of the most widely
researched areas, the available systematic
reviews do not always provide clear direction for
the clinician in choosing which patients to treat
in which way. An example is found in a system-
atic review of professionally applied fluorides in
which virtually all of the vehicles tested were
shown to be effective, but the clinician was still
12 Evidence-Based Dentistry 169
left with no clear direction as to which patients
should receive fluorides, what fluoride product
to use, and how long they need to be provided to
each patient.14 The clinician must still rely on
professional judgment in areas such as the trade-
off between the cost of treatment, on the one
hand, and the likelihood that the patient will
develop caries in its absence. It is also possible
that the experimental subjects in the studies on
which the systematic reviews are based are fun-
damentally different from the patients in a par-
ticular dentist’s practice. Some patients may be
at very low risk for certain conditions, so the
appropriateness of using some preventive meth-
ods on a frequent basis may be questionable.
Other patients may be at higher than average
risk and may need more aggressive treatment.
Evaluation of these types of subtle distinctions is
not common in the current scientific literature,
and thus recommendations by systematic
reviews on these dimensions are rarely available.
Nevertheless, the shortcomings of the literature
that are identified in scientific reviews can help
to define the future research agenda and to
address the current gaps in knowledge, so that
the level of specificity possible in future system-
atic reviews will make them even more valuable
to clinicians in the future.
LIMITATIONS OF EVIDENCE-BASED
DENTISTRY
EBD is an important evolution in the con-
tinuing drive to provide the right care, to the
right patient, at the right time. It is not an infal-
lible prescription for what to do in all clinical
situations, and in many areas the underlying
clinical research has simply not been done.
Nevertheless, the research base will continue to
develop, and the approach provides a workable
method to give the busy clinician a rigorous
review and balanced summary of the evidence
available up to the present, in a form that is
readily accessible and digestible. This body of
underlying evidence and systematic summaries
will grow rapidly and should be an ever-increas-
ing part of both clinical teaching and everyday
clinical practice.
Systematic reviews are not always unambigu-
ous, and they are always open to reinterpreta-
tion and revision.20 As with all of science, new
evidence or reinterpretation of current evidence
170 Dental Practice
may in the future change the conclusions of a
review. It must further be remembered that
there is not a single truth that, once discovered,
will remain so forever. By its very nature, science
is always open to revision and reevaluation.
Therefore, EBD, based as it is firmly on science,
is always open to revision. These facts place sig-
nificant demands on the clinician. On the one
hand, it is imperative that the current best prac-
tices, as supported by rigorous science and sys-
tematic reviews when available, be carefully
considered when making treatment decisions.
On the other hand, such practices emphatically
must not be taken as immutable fact and used
without further thought throughout a career.
The competent clinician must constantly look
for systematic reviews to find new evidence as it
becomes available and watch for signs of
changes in what had previously been consid-
ered the best evidence.
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 13 Research Designs in Oral
Epidemiology
CAUSALITY AND RISK
NONEXPERIMENTAL STUDY DESIGNS
EXPERIMENTAL STUDY DESIGNS
Choice of Population in Which the Trial Will Be
Conducted
Adequacy of the Numbers of Subjects
Comparability of Study and Control Groups
Numerous books have been written about
research design and the characteristics of good
research. This is not one of them, but we do set
out in this chapter to give a bare-bones presenta-
tion of the essentials of valid research reports.
This coverage is intended to permit the reader to
make good sense of epidemiologic studies, espe-
cially clinical trials, and of other studies involv-
ing human beings.
Epidemiology is the study of health and dis-
ease in populations, and of how these states are
influenced by heredity, biology, physical envi-
ronment, social environment, and ways of liv-
ing. Some definitions extend the meaning to
include the application of this study to control
health problems.14 Epidemiologic studies can
first be classified either as descriptive, meaning
that the data only describe the distribution of a
condition in a population and no specific
hypothesis is tested, or as analytic, meaning that
the data collection and analysis are designed to
answer a particular question. Descriptive and
most analytic studies are observational; that is,
they observe outcomes without intervening
to affect them. Analytic studies in epidemiology
look at people with and without the disease in
question (the effect or outcome) and with and
without exposure to the putative influences that
may increase the risk of disease (the exposure).
The clinical trial, an experimental design to
test the efficacy of a preventive-control agent or
treatment procedure in humans, is an aspect of
Use of a Placebo in the Control Group
Control of Operational Procedure
Examiner Reliability
Duration of the Trial
Statistical Analysis
Ethical Considerations
analytic epidemiology sometimes classified
separately as experimental epidemiology. The
clinical trial is also an interventional design; that
is, something is intervening in the natural his-
tory of a condition in an effort to give a benefi-
cial outcome.
Good research demands careful, sometimes
exhaustive planning. Every study, no matter
how modest, needs a protocol, which is a writ-
ten plan encompassing the purpose and the
detailed operation of the study. The essential
elements of a protocol are listed in Box 13-1.
A protocol demands careful thinking through
of a project, a process that aids its design and
also helps the researchers to anticipate potential
problems. It also simplifies the writing of a final
report, because the protocol forms the basis of
the report.
CAUSALITY AND RISK
Causality, meaning that a certain exposure
results in a particular outcome, can only be
demonstrated unequivocally within the experi-
mental study design of a clinical trial (discussed
in a later section). Because clinical trials cannot
be conducted on many topics for both practical
and ethical reasons, causality in the study of dis-
ease usually must be imputed from studies with
nonexperimental designs. Criteria by which
a conclusion of causality can be reached
from nonexperimental epidemiologic analyses,
173
174 The Methods of Oral Epidemiology
BOX 13-1 Essential Features of a Protocol for Research With Humans
●
A precise definition of the research problem, the
reasons for undertaking the research, and a review
of pertinent literature.
●
Objectives of the study or hypotheses to be tested.
A hypothesis is a conjecture cast in a form (the null
hypothesis) that will allow it to be tested and refuted
if it is false.
●
Population to be studied, including its selection,
source, size, method of sampling, and method of
allocation to groups (if a clinical trial).
●
Data to be collected, including a description of each
item needed to accomplish the objectives or to test
the hypotheses.
●
Procedures to be carried out, with details of exactly
how the needed data will be obtained from the
participants in the study and by whom.
BOX 13-2 Criteria for Inferring Causality From Observational Studies (the Bradford Hill Criteria)3
The following conditions must he satisfied before a
particular exposure can be accepted as the cause of a
disease:
●
Time sequence of events: To be causal, an
exposure must precede the occurrence of the
disease. Demonstration of this temporal sequence
requires longitudinal study. This is the only
condition in this list that is absolute, a sine qua non.
●
Consistency of association: If there are a good
number of studies on whether a particular exposure
is a cause of a disease, and if all of them produce
fairly similar positive results, it is more likely that the
factor is causal.
●
Strength of association: In valid studies, the stronger
the association between exposure and outcome, the
more likely it is that the association is causal.
known as the Bradford Hill Criteria after the
British statistician who developed them, were
suggested in 19653 and have become well
accepted over the years. The original Bradford
Hill criteria have evolved over the years and are
summarized in Box 13-2 as they are usually
understood today.
Analytic studies, in contrast to descriptive
studies, have the general aim of seeking out
cause-and-effect associations. Because analytic
observational studies cannot directly address
cause and effect, however, they seek to quantify
●
Data collection methods, with examples of all data
collection forms or computer methods of data
collection and a list of all necessary supplies,
equipment, and instruments.
●
Plans for data processing and analysis, including how
the data get from field collection to computer,
computer file organization, and statistical
distributions to be examined.
●
Time schedule for planning, procurement of informed
consent from study subjects, data collection and
analysis, and report writing.
●
An assessment of any ethical issues involved in the
study and certification that the necessary institutional
human subjects clearance has been obtained.
●
Specificity of association: If a given exposure is
related to other diseases as well as the disease in
question, it is less likely to be seen as causal.
However, lack of specificity by itself does not justify
rejecting causality (e.g., tobacco is nonspecific in its
effects but is clearly a causal factor in many of them).
●
Degree of exposure (dose response): If an exposure
is causal, then the risk of disease should be related to
the degree of exposure. An exception could be
exposure to a toxin with a threshold effect.
●
Biologic plausibility: The association must make
biologic sense from our knowledge of the disease. It
follows that the better understood a disease is, the
more stringent this criterion can become.
the degree of disease risk in specified circum-
stances. Risk is the probability that a specified
event will occur, for example, that an individual
will exhibit a disease or die within a stated
period of time or by a particular age.14
The criteria listed in Box 13-2 are not all
imperative; in fact the only absolute among
them is the time sequence—exposure must pre-
cede outcome. In many exposure-outcome rela-
tionships there are factors that both researchers
and clinicians think play a role in causing a dis-
ease but which do not satisfy all these criteria. If

researchers had to proceed with just the dichoto-
mous judgment of whether a factor is or is not
involved in causing a disease, our knowledge of
disease causation and development would be
seriously hindered. The concept of a risk factor
permits quantification of the degree of impor-
tance of a particular factor in the development of
a disease; some causal factors are more impor-
tant than others.
A risk factor is broadly defined as an attribute or
exposure that is known, from epidemiologic evi-
dence, to be associated with a health condition
considered important to prevent.14 Although the
term risk factor is applied loosely in the literature,
modern usage ascribes a strong causal role to a
risk factor: it is either part of the causal chain or is
something that brings a person into contact with
the causal chain. (An example of the latter situa-
tion is an occupation that requires handling toxic
materials. The occupation itself is not a risk factor
for toxicity, but because it brings a person into
contact with toxic materials, which are the risk
factors, it does increase the chance of disease.) We
prefer the following more complete definition of
risk factor:
An environmental, behavioral, or biologic factor confirmed by
temporal sequence, usually in longitudinal studies, which if
present directly increases the probability of a disease occur-
ring, and if absent or removed reduces the probability. Risk
factors are part of the causal chain, or expose the host to the
causal chain. Once disease occurs, removal of the risk factor
may not result in a cure.2
Part of the concept of a risk factor is that it
can be modified: people can stop smoking, lose
weight, change to a healthier diet, improve their
oral hygiene. The identification of risk factors
for a disease then allows the potential for pre-
vention by removing or modifying the risk fac-
tors. As examples, smoking is a risk factor for
lung cancer; poor oral hygiene is a risk factor
for gingivitis. In both instances, removing or
modifying the risk factor reduces the risk of
disease, although neither exposure is a sole
cause of the disease.
As stated in this definition, a risk factor for a
disease must be demonstrated as such longitu-
dinally. This is because confirming the neces-
sary time sequence—that is, ensuring that
exposure to the risk factor occurs before the dis-
ease outcome—can nearly always be demon-
strated only longitudinally. This time sequence
13 Research Designs in Oral Epidemiology 175
BOX 13-3 Criteria to be Met to Accept a Given
Exposure as a Risk Factor for a Particular Disease13
●
Time sequence: The exposure must precede the
occurrence of the disease.
●
Statistical association: The exposure must covary
with the disease; that is, that the frequency of the
disease must be observed to differ by category or
value of the exposure.
●
Absence of error: The observed association must
not be the result of error, whether that be bias,
sampling error, analytic errors, or the intrusion of
other extraneous factors.
is one of three criteria that must be met before
we can suggest that a particular exposure is a
risk factor for a particular disease (Box 13-3 lists
the criteria for identifying a risk factor. Box 13-2
gives the criteria for imputing a cause.) The ulti-
mate test of a risk factor is that, if exposure to it
is reduced, the risk of subsequent disease
diminishes. As an example, quitting smoking
reduces the risk of a heart attack.
What if a suspected risk factor cannot be con-
firmed as such because the necessary longitudi-
nal studies are impractical or unethical? The
factor may be classed as a risk indicator, defined
as a factor shown to be associated with a disease
in cross-sectional data and assumed, on theo-
retical grounds, to play some causal role.15
Research experience has shown that risk indica-
tors which emerge from cross-sectional studies
can disappear in a more rigorous longitudinal
analysis, so without longitudinal assessment it
cannot be known whether a risk indicator is or
is not a true risk factor. As would be expected,
many more risk indicators for oral diseases than
true risk factors have been identified.
A risk marker is an attribute or exposure that
is associated with the increased probability of
disease although it is not considered part of the
causal chain. A risk marker can also be called a
risk predictor when included in predictive statis-
tical models. Some immutable characteristics of
a person or group—namely, age, gender, and
race or ethnicity—can influence disease occur-
rence, progression, or outcome. These attributes
do not fit the concept of a risk factor because
they are not modifiable. Although they can be
176 The Methods of Oral Epidemiology
useful in statistical models whose purpose is to
predict disease occurrence, they clearly are of no
use when considering disease prevention based
on control of risk factors. The literature is unfor-
tunately muddled about what to call these
attributes. We suggest the term demographic risk
factors to refer to these immutable influences. In
addition to age, gender, and race or ethnicity,
socioeconomic status is usually considered a
demographic risk factor. Theoretically it can be
modified, but in practice this is hard to do.
NONEXPERIMENTAL STUDY DESIGNS
The collection of data to be used for descriptive
purposes is commonly called a survey (see
Chapter 4). Surveys record the prevalence of vari-
ous conditions, meaning the number or pro-
portion of persons in the population who
exhibit a condition at any given time. (Data
from national surveys in the United States are
reported in Chapters 19-22.) Although surveys
are important in assessing trends in health and
disease, the field of oral epidemiology encom-
passes much more than surveys.
At the most basic level, epidemiologic study
designs are cross-sectional or longitudinal. A cross-
sectional study is one in which both exposure to
risk factors and the health outcomes in a group
of people who are, or are assumed to be, a sam-
ple of a particular population (a “cross section”)
are assessed at the same time. A longitudinal
study is one in which the same group of people
is studied on two or more occasions so that inci-
dence, the change in a condition over time, can
be assessed. A survey collects cross-sectional
data. Comparison of trends by examining the
results of a sequence of surveys, even if the same
study protocols are used in all of them, is still a
cross-sectional comparison because different
people are examined in the different surveys.
Longitudinal studies require at least two
series of measurements among the same people
at different times to determine the progress of
the condition over the specified time period.
Such a study is also an incidence study.
Sometimes an analytic study can be cross-
sectional, such as when several cross-sectional
studies are performed over a period of time for
analytic purposes. An examination of mortality
trends, for example, must be cross-sectional
(obviously it cannot be the same people who
die on different occasions!). A comparison of
the prevalence of dental caries in today’s sixth-
graders with that of sixth-graders 10 years ago
must be a cross-sectional study, although it
could also be an analytic one; again it is obvious
that different persons are studied each time. But
if all the children originally in first grade in a
school system are studied periodically until
they finish sixth grade some years later, the
study is longitudinal because the same children
are seen on several occasions.
Analytic studies are either prospective (look-
ing forward) or retrospective (looking backward).
Prospective studies collect information on an
exposure of interest and compare eventual out-
comes, whereas retrospective studies begin with
the outcome of interest and probe back for
exposure information. A cohort study is a
prospective design: a cohort is a group of people
from whom data are collected longitudinally.
Members of a cohort often have some particular
characteristic in common, frequently age; thus,
the expression “the 1955 birth cohort” means
all persons born in 1955. In cohort studies,
some individuals will have the exposure of
interest and some will not, and some will have
the outcome of interest and some will not. This
permits the computation of relative risk, the
chance that the outcome will occur in an
exposed person compared to the risk among the
unexposed.14
Science has long viewed retrospective studies
as being inherently of poorer quality than
prospective studies. This view is unjustified,
however, because many unusual conditions or
conditions that develop over a long period of
time can only be studied realistically through
retrospective designs. Indeed, the noted epi-
demiologist Rothman considers the develop-
ment of the retrospective study design to be one
of the major advances in epidemiologic meth-
ods in recent years.20 The principal retrospective
design is the case-control study, in which people
who have a given condition (“cases”) are com-
pared to, and sometimes matched with, people
who do not have the condition (“controls”) but
who may be similar with regard to some other
characteristics. The exposures of interest are
then sought in the past of the participants. This
design permits the derivation of an odds ratio, a
numerical statement of probability very similar
to relative risk.

Case-control studies must be planned
thoughtfully, because the characteristics on
which the groups are matched (e.g., ethnic
group) cannot be analyzed further as possible
etiologic factors. Case-control studies can
demonstrate risk indicators for a disease, but
the retrospective design means that risk factors
cannot be identified in this way. Risk factors for
a disease can be confirmed only through cohort
or experimental study designs.
An ecologic study is an analytic study in which
data for both exposures and outcomes come
from the population rather than from individu-
als. For example, studies addressing the ques-
tion of whether water fluoridation is related to
hip fracture experience (i.e., suggesting that
fluoridation is a risk factor for hip fracture) have
used community data for both water fluorida-
tion (the exposure) and for hip fractures (the
outcome) to derive a relationship.11,21 Such
studies are relatively quick and inexpensive
because they avoid sampling, interviewing, clin-
ical examinations, or access to individual med-
ical records. Their weakness, however, is that
they cannot be certain that the people with the
outcome condition (in this case, the hip frac-
ture) are the same ones who had the exposure
(drank fluoridated water). This weakness is
often called the ecologic fallacy. Ecologic studies
can be useful, though usually they are not defin-
itive. They have a clearer role when a variable
under consideration, for example, community
income level, is by definition a group measure
rather than an individual one.
All of these study designs are nonexperimen-
tal and noninterventional, meaning that they
study conditions as they occur rather than
manipulate conditions in the manner of a clas-
sical laboratory experiment. However, there are
experimental designs in epidemiology that are
used to test the efficacy or effectiveness of a ther-
apeutic drug, a preventive material, or a treat-
ment regimen.
EXPERIMENTAL STUDY DESIGNS
In medical terminology, clinical trials are carried
out among patients, frequently hospital inpa-
tients, and field trials are carried out among peo-
ple in the community who may not necessarily
be patients. This medical model does not trans-
fer well to dentistry, where the definition of a
13 Research Designs in Oral Epidemiology 177
patient is less clear-cut and only a small part of
dental care is provided in hospitals. The term
clinical trial tends to be loosely applied in den-
tistry to both types of study, so we will use it in
this chapter when describing research principles
common to both clinical trials and field trials.
We will use the term field trial (sometimes called
a community trial, or an effectiveness study) only
when specific reference to a field trial is needed.
A clinical trial is a controlled experimental
study or group comparison, based on epidemi-
ologic principles and designed to test the
hypothesis that a particular agent or procedure
favorably alters the natural history of a disease.
The group receiving the agent or regimen under
study is the test group, sometimes called the
experimental or study group, whereas a compara-
ble group not subject to the agent or regimen is
the control group. Clinical trials compare results
in two or more samples of a single population,
divided into groups that are essentially similar
(in distribution of age, sex, race, socioeconomic
status, and previous disease experience). The
aim is to ensure that the only difference
between the groups is the fact that the test group
receives the treatment under study whereas the
control group does not.
Much of the basis for preventive procedures
in dentistry has come from the results of clinical
trials, although the quality of trials described in
the dental literature varies from excellent to
poor. The reader can judge the validity of a trial
by determining how closely the report adheres
to certain principles in its conduct. These princi-
ples are described in brief in the following
sections.
Choice of Population in Which the Trial
Will Be Conducted
Choice of population should be determined by
the purpose of the trial. If the prime purpose of
a clinical trial is to test the efficacy of a particular
agent, that is, whether it works or not, then the
most favorable conditions should be created to
show that it does work. For that reason, the
project should be conducted with subjects who
are selected for their susceptibility to the disease
or condition. This means that a population of a
specific age range is usually chosen deliberately,
because many oral diseases are age specific (see
Chapters 19-23). Sex, race, socioeconomic sta-
tus, and geographic location are other factors
178 The Methods of Oral Epidemiology
considered in the choice of a study population
for efficacy trials. If, however, the purpose is to
assess the effectiveness of an agent under every-
day conditions, then broad community popula-
tions, those with varying degrees of the disease
or condition under study, should be chosen.16
Confusing the purposes of trials can lead to the
error of generalizing the results of efficacy trials
conducted in special populations with unusual
disease distributions, such as institutionalized
people, to the general population.
Adequacy of the Numbers of Subjects
Loss of subjects during a prospective clinical trial
is a fact of life and must be planned for. If the
numbers of subjects in the groups are not
large enough to begin with, at the end of the trial
the researcher will be left with too few subjects
to be able to show by statistical logic whether it
is likely that an observed difference between the
groups is real or a chance result. The result may
then be that a real difference cannot be detected,
and an agent that in fact is effective will not seem
to be so. This issue relates to data analysis and
the conclusions from the trial, and is discussed
more fully later in this chapter.
Comparability of Study and Control
Groups
The randomized trial, always the most elegant
design for efficacy studies4 and a cornerstone of
evidence-based dentistry (see Chapter 12), is
one in which group similarity is achieved by
random allocation of subjects to the study and
control groups. Random allocation means that
each participant has an equal chance of being
assigned to either the study or the control
group. Statistical probability is such that the
assumption can then be made that bias is not
intruding and that at the end of the trial any dif-
ferences between the groups can be attributed
only to the agent under study. Any uncontrolled
variables influencing the outcome, which are
usually undetected by the researchers, are likely
to affect subjects in both groups equally and
therefore not to affect the relative differences
between the groups.
The principle of random allocation is simple,
although it is a carefully planned and controlled
procedure. Random allocation is not haphazard
assignment or one based on volunteering or self-
selection. A statistician can further improve the
probability of establishing comparable groups
by stratification, which means that before alloca-
tion the base population is separated by those
factors known or thought to influence disease
occurrence (usually age, sex, race, socioeco-
nomic status, and previous disease experience).
Subjects from each stratum are then randomly
allocated to study and control groups.
Nonrandomized trial designs are not uncom-
mon in the dental literature.18,19 Although they
are weaker than randomized designs, sometimes
practical considerations dictate their use. For
example, the landmark Vipehölm study on diet
and caries (see Chapter 28) was a prospective
study, but participants were assigned to groups
on a convenience basis rather than by random-
ization. This could have influenced the results to
some extent. Some studies dispense with a con-
trol group altogether and determine efficacy by
comparison with historical controls; that is, they
use a before-and-after design in which disease
levels at the end of the project are compared
with those at the beginning.10 The weakness in
this design is that uncontrolled change could
take place during the trial to invalidate results.
For example, in a trial of a fluoride mouthrinse,
children in sixth grade at the completion of a
3-year trial may have brushed with fluoride
toothpaste more often than did the sixth-graders
examined at the beginning of the trial. Without
use of a concurrent control group it is impossi-
ble to tell if beneficial outcomes were due
entirely to the mouthrinse or were due at least in
part to the additional toothpaste use.
Before-and-after trials are often called demon-
strations, intended to “demonstrate” the value of
accepted preventive measures.12 Presenting a
case for the scientific validity of demonstrations
can get complicated,9,10 although it is worth not-
ing that the pioneering Grand Rapids fluorida-
tion trial used this design (see Chapter 25).
A major threat to the validity of a before-and-
after design comes from undetected sociodemo-
graphic change in the population under study
during the period of the trial.
Some studies have used a comparison group,
defined as any group to which the study group
is compared and a term that too often is used
synonymously with control group.14 It is less con-
fusing, however, if the term control group is
reserved for randomized controls and the term
comparison group is used for nonrandomized

comparisons. Examples of comparison groups
are the control communities used in fluorida-
tion field trials (see Chapter 25). Some compar-
ison groups can be similar to study groups and
thus permit fairly valid comparisons, but others
are so far removed from the study group that
they serve little purpose.
Certain types of trial use a crossover design, in
which subjects serve as their own controls. Each
subject receives an active treatment for a specific
time and a placebo (or no treatment) during a
control period. Crossover designs are useful in
short-term trials (weeks or months, rather than
years) for preventing reversible conditions like
gingivitis or calculus accumulation but are
unsuitable for caries prevention trials because
the time needed for new lesions to develop is
too long. They are also not appropriate for test-
ing of regimens that have a carryover effect,
because the effects of the treatment phase could
influence responses during the nontreatment
phase. Crossover designs are also inappropriate
when the tested regimen may produce a perma-
nent effect, when test agents may be retained at
the site of action for prolonged periods, or
when conditions may naturally undergo a rapid
change in prevalence, incidence, or morbidity.
The principal advantage of a crossover design is
that results are not affected by variations in
response among participating subjects.
In studying efficacy trials, readers should
take care not to confuse the need to carefully
select the study population with the necessity to
randomly allocate the individuals in that popu-
lation to the study and control groups.
Use of a Placebo in the Control Group
A placebo is a material or formulation like the
test product but without the active ingredient,
such as a toothpaste that feels and tastes like a
fluoride toothpaste but contains no fluoride.
The purpose of using a placebo in a trial is to
keep subjects unaware of whether they are in
the test or control group (a blind study), so that
their health behavior will not be consciously or
unconsciously affected by group allocation.
Bias, which is systematic though usually uncon-
scious error, can affect examiners as well: an
examiner who expects a product to be effective
may unconsciously apply stricter criteria for
caries in a control group if he or she knows
which children are in which group. Examiners
13 Research Designs in Oral Epidemiology 179
therefore also should not know the group allo-
cation of subjects. When neither participants
nor examiners know the group allocations, the
trial is termed double-blind.
Use of a placebo is inherently impossible in
some instances, such as in trials of water fluori-
dation (where the fluoridating community is a
matter of public record), fissure sealant (where
sealant visibility determines the outcome), or
dental health education (where the control at
best is a comparable group that receives no pro-
gram, a passive control). Placebos raise ethical
issues, because it is usually considered unethi-
cal to deny established beneficial products to
trial participants. If a manufacturer wants to test
fluoride toothpaste with a stronger formulation
than is standard, for example, the control group
does not use a nonfluoride toothpaste but
rather a standard-strength product. This is
called a positive control; the results then compare
the effects of the new product with the effects
of the old one. Because the difference between
these two groups would be expected to be
less than if a placebo were used, the trial needs
larger numbers of participants to permit any
true difference to be shown.
The ethical issue is recognized, but the weak-
ness of efficacy trials without controls is that we
never know if using a tested product in a public
health program is any better than having no
program. In an age of low caries experience and
extensive fluoride exposure (apart from any that
may be associated with the test product), that
can be a fair question.
Control of Operational Procedure
An efficacy study, designed to answer the ques-
tion of whether a particular agent or regimen
works or not, must give the test agent every
chance to succeed. Susceptible populations are
chosen for the trial, participants are randomly
allocated to test and control groups, and double-
blind conditions prevail. But in addition the
researchers need to be sure that the agent is used
as intended. If it is a professionally applied agent
or a treatment regimen, the protocol must spec-
ify precisely how the agent will be used, for how
long, how often, at what concentration, and by
whom. A placebo, or positive control, would be
applied the same way. If a self-applied agent
is being tested, such as a mouthrinse, the proto-
col should call for the agent to be used under
180 The Methods of Oral Epidemiology
professional supervision. It is the researchers’
task to ensure that the protocol is adhered to
throughout the course of the study.
In an effectiveness trial, the agent or treatment
can be used as it normally would. That means
that professionals are given instructions in the
use of a procedure or participants are given
the rinse to take home and use as instructed.
Therefore there is less certainty in an effectiveness
trial that the material has been used as intended,
but part of the aims of an effectiveness trial is to
evaluate how the material works under everyday
conditions. In operational control, as in other
aspects of a trial, the purpose of the study must
be kept in mind.
Examiner Reliability
Examiners in clinical trials must record disease
that has developed over a relatively short period
of time. This requirement forces the examiner to
diagnose disease at an early stage of its develop-
ment, which increases the risk of error. In caries
trials, the most troublesome form of error is
that an early lesion classed as carious at the first
round of examinations may be classified as
sound in subsequent examinations, a negative
reversal, more commonly referred to just as a
reversal. Reversals are virtually unavoidable in
any form of sequential diagnosis,17 although
they should remain a fairly small proportion of
all diagnoses. The ways of dealing with reversals
in data analysis are discussed in Chapter 15,
and further discussion of examiner reliability is
found in Chapter 14.
The validity of clinical trial results depends
heavily on the reliability of the examiner(s). This
factor is usually referred to as intraexaminer relia-
bility (i.e., within-examiner consistency) or the
ability of an examiner to record the same condi-
tions the same way over time. Most examiners
with training and experience can develop an
acceptable degree of intraexaminer consistency.
Consistency between different examiners,
interexaminer reliability, is more difficult to
achieve, even when the examiners train together
from the same written criteria. It is best to use
one well-qualified examiner, but large-scale
studies usually require more than one examiner,
and multicenter trials certainly do. In such cases
the examiners should undergo a period of train-
ing to bring their diagnostic standards as close
together as can possibly be managed. This train-
ing procedure is referred to as standardization.
When one of the group serves as the “gold stan-
dard” examiner and the training is to enable
other examiners to record similarly, the term cal-
ibration can be applied.
Radiographs can be helpful in a trial, but the
same issues of examiner consistency are pres-
ent. Diagnostic criteria must be established, and
intraexaminer and interexaminer consistency
maintained with radiographic interpretation
just as with clinical examinations. Given the
logistic and ethical issues that also arise, use of
radiographs is usually not recommended in
field trials.8 That is not necessarily the case in
clinical trials in a dental school setting, where
patients may undergo radiography anyway in
the course of treatment.
Duration of the Trial
Clinical trials must be continued long enough to
permit detection of new disease or extension of
lesions already present. For caries trials, the min-
imum duration is usually 2-3 years, although
precise timing depends on the purposes of the
trial.7 The longer the trial, the more expensive it
is, so trade-offs are again required. The FDI
World Dental Federation suggested in 1977 that
trials of plaque-inhibiting agents could be as
short as 8-21 days,6 but that guideline was for
plaque measurements only. The FDI also recom-
mended that studies of calculus-preventing
agents should last at least 90 days for supragingi-
val calculus and longer for subgingival calculus.
The American Dental Association requires that
plaque-inhibiting agents for which the associa-
tion’s seal of approval is sought (see Chapter 29)
demonstrate gingivitis reduction as well as
plaque reduction; it requires such trials to be at
least 6 months long.1
Statistical Analysis
It is not our purpose to cover the methods of
statistical analysis in this text, because numer-
ous excellent biostatistics textbooks are avail-
able. One particular analytic issue that can
bother readers of the literature, however, is that
of the relationship between statistical signifi-
cance and clinical importance. This issue is worth
some discussion here.
A clinical trial to test a preventive agent or
treatment regimen begins with a null hypothesis
(i.e., the proposition that there is no difference

in disease experience between the test and con-
trol groups). When large differences between
test and control groups are expected, the groups
can be smaller than when small differences are
expected. In either case, groups must be large
enough (i.e., the trial must have sufficient statis-
tical power) to permit the observed differences in
disease increment between test and control
groups to be reasonably tested for statistical sig-
nificance, which is the probability that the
observed results are due to chance rather than to
the efficacy of the tested product or regimen.
Chance in this context means that even with
random allocation one group had more disease-
susceptible or disease-resistant individuals. (It
does not mean the probability of a chance result
because of poor design or sloppy conduct of the
study!) Such differences are not always apparent
when the groups are compared following alloca-
tion, but if it is apparent immediately after allo-
cation that the groups differ in some important
respect, the groups can be disbanded and the
allocation procedure repeated.
When comparing the observed results in a
clinical trial, it has been traditional to accept
5% (sometimes stated as 0.05) as the outer
limit of acceptable statistical significance. The
statement p = 0.05 thus means that the risk of
accepting the observed difference between the
groups as real when actually it is due to chance
is 5 in 100. In this case, the 5% chance of falsely
accepting that a regimen is effective is termed
type I error and the Greek letter α (alpha) is the
probability of making a type I error. To offer
greater assurance that an observed difference is
real, investigators may set α at 1% (p = 0.01),
although the trade-off here is that larger group
sizes are necessary.
However, the selection of a small α level does
not protect investigators from the possibility of
failing to identify an effective agent or regimen.
If the group size is too small, it is possible to
conclude mistakenly that a treatment has no
effect when in fact it really does. This latter mis-
take is known as type II error, and the probabil-
ity of making a type II error is signified by the
Greek letter β (beta).
The chance of detecting a true effect, if it
exists, is denoted as the power of the test and is
defined as 1 − β. Power is dependent on (1) the
magnitude of the difference observed between
the two treatments, (2) the number of subjects
13 Research Designs in Oral Epidemiology 181
in each group, (3) the population variance, and
(4) the α level chosen. If the findings of a study
are negative (meaning that the null hypothesis
cannot be rejected), the power of the test indi-
cates how confident one can be that the find-
ings are truly negative. The goal in considering
power when calculating group sizes is to
enhance the chances of finding effects if they
really do exist.
The power of a test is critically important in
trials using a positive control, for example,
those testing a higher-concentration fluoride
toothpaste against the positive control of a stan-
dard fluoride product. Differences in caries
increments between the groups are likely to be
small. If the investigators judge that differences
as small as 15% between groups are clinically
meaningful, they will need to be able to
demonstrate that differences this small are sta-
tistically significant. The group sizes then have
to be extremely large.5 Otherwise, with smaller
groups, the researchers may falsely conclude
that the regimens were equivalent because they
failed to demonstrate statistical significance,
when in fact the chance of demonstrating such
significance, or the power of the test, was small
to begin with.
In a well-conducted study, type I errors usu-
ally arise from the fact that sometimes the ran-
dom allocation process results in bias in the
composition of the groups. In a less well-
conducted study, it can come from an absence
of random allocation and from lack of blind-
ness in either examiners or participants. In an
otherwise well-conducted study, type II errors
typically come from group sizes that are too
small to permit demonstrating statistical signifi-
cance when clinical differences are apparent
(i.e., the trial is underpowered). Imprecise diag-
nosis by examiners, in which a lot of random
error will result in high error variance, can also
lead to type II error. In a trial in which there has
been no random allocation, the assumptions
underlying the statistical probability tests have
been violated, so the p values presented in such
reports have little value.
Overcoming problems of sample size requires
more care than simply making study groups as
large as possible. The reason is that, when groups
are large, the most trivial difference in disease
increment between them will reach statistical sig-
nificance. This can be misleading if there is no
182 The Methods of Oral Epidemiology
clinical importance to the difference observed;
therapeutic importance cannot be concluded
simply because statistical significance has been
determined. Using sample sizes larger than nec-
essary is also inefficient; each additional subject
in a study adds extra expense, consuming funds
that could be used to conduct other important
studies.
Ethical Considerations
Group sizes in a clinical trial should not be
unduly large, because it is unethical to involve
participants in research when their involvement
is scientifically unnecessary and needlessly
exposes them to the inconvenience and possi-
ble risks of participation. Humans taking part in
clinical trials must give informed consent,
which means providing a written acceptance
that the participant understands the conduct of
the trial and the nature of any risks involved.
Researchers must certify in the report of the trial
that the study protocol has been accepted
by their institution’s review board, which any
institution conducting research is required to
maintain. If the study raises special issues (e.g.,
if it includes illiterate or mentally retarded peo-
ple), extra explanations are usually required in
the report. Additional explanation of how the
rights of participants have been safeguarded
may also be needed if the study is conducted in
a developing country that does not have the
same rigorous standards for human subject
protection as do the developed nations.
REFERENCES
1. American Dental Association, Council on Dental
Therapeutics. Guidelines for acceptance of chemothera-
peutic products for the control of supragingival plaque
and gingivitis. J Am Dent Assoc 1986;112:529-32.
2. Beck JD. Risk revisited. Community Dent Oral
Epidemiol 1998;26:220-5.
3. Bradford Hill A. The environment and disease: Association
or causation? Proc R Soc Med 1965;58:295-300.
4. Cochrane AL. Effectiveness and efficiency: Random reflec-
tions on health services. London: Nuffield Provincial
Hospitals Trust, 1971:20-5.
5. Conti AJ, Lotzkar S, Daly R, et al. A 3-year clinical trial to
compare efficacy of dentifrices containing 1.14% and
0.76% sodium monofluorophosphate. Community
Dent Oral Epidemiol 1988;16:135-8.
6. Fédération Dentaire Internationale, Commission on
Classification and Statistics for Oral Conditions.
Principal requirements for controlled clinical trials in
periodontal diseases. Int Dent J 1977;27:62-76.
7. Fédération Dentaire Internationale, Commission on
Oral Health, Research and Epidemiology. Principal
requirements for controlled clinical trials of caries
preventive agents and procedures. Int Dent J 1982;32:
292-310.
8. Horowitz HS. Ethical considerations of study partici-
pants in dental caries clinical trials. Community Dent
Oral Epidemiol 1976;4:43-50.
9. Horowitz HS, Meyers RJ, Heifetz SB, Driscoll WS. Eight-
year evaluation of a combined fluoride program in a
nonfluoride area. J Am Dent Assoc 1984;109:575-8.
10. Horowitz HS, Meyers RJ, Heifetz SB, et al. Combined
fluoride, school-based program in a fluoride-deficient
area: Results of an 11-year study. J Am Dent Assoc
1986;112:621-5.
11. Jacobsen SJ, Goldberg J, Cooper C, Lockwood SA. The
association between water fluoridation and hip frac-
ture among white women and men aged 65 years and
older. A national ecologic study. Ann Epidemiol
1992;2:617-26.
12. Klein SP, Bohannan HM. The first year of field activities
in the National Preventive Dentistry Demonstration
Program. Rand Report No. R-2536/1-RWJ. Santa Monica
CA: Rand Corporation, 1979.
13. Kleinbaum DG, Kupper LL, Morgenstern H. Epidemio-
logic research: Principles and quantitative methods.
Belmont CA: Lifetime Learning Publications, 1982:
25-34.
14. Last JM, ed. A dictionary of epidemiology. 4th ed. New
York: Oxford University Press, 2001.
15. Locker D, Leake JL. Risk indicators and risk markers for
periodontal disease experience in older adults living
independently in Ontario, Canada. J Dent Res 1993;72:
9-17.
16. O’Mullane DM. Efficiency in clinical trials of caries pre-
ventive agents and methods. Community Dent Oral
Epidemiol 1976;4:190-4.
17. Radike AW. Examiner error and reversals in diagnosis.
In: Proceedings of the conference on the clinical testing
of cariostatic agents. Chicago: American Dental
Association, 1972:92-5.
18. Ringleberg ML, Conti AJ, Webster DB. An evaluation of
single and combined self-applied fluoride programs in
schools. J Public Health Dent 1976;36:229-36.
19. Ripa LW, Leske GS, Levinson A. Supervised weekly rins-
ing with a 0.2% neutral NaF solution: Results from a
demonstration program after two school years. J Am
Dent Assoc 1978;97:793-8.
20. Rothman KJ. Modern epidemiology. Boston: Little
Brown, 1986:3.
21. Suarez-Almazor ME, Flowerdew G, Saunders LD, et al.
The fluoridation of drinking water and hip fracture hos-
pitalization rates in two Canadian communities. Am
J Public Health 1993;83:689-93.
 14 The Measurement of Oral Disease
EPIDEMIOLOGY: AN INTRODUCTION
Early Studies
The Concept of Measuring Disease
SAMPLING FROM HUMAN POPULATIONS
METHODS OF MEASURING ORAL DISEASES
Counts
Proportions
Why do some patients have serious periodonti-
tis whereas apparently similar patients do not?
Why does a child who seems to eat candies all
day not get caries? Frequently there is no obvi-
ous answer. That branch of scientific inquiry
which seeks to find order among these appar-
ently haphazard patterns of disease is epidemiol-
ogy. Epidemiology is defined as the study of
health and disease in populations, and of how
these states are influenced by heredity, biology,
physical environment, social environment, and
ways of living.
Epidemiologic study requires that disease be
measured quantitatively. This chapter describes
the philosophies that underlie disease measure-
ment and some of the procedures used. These
methods are fundamental to the conduct of
research, and they can also be of value to practi-
tioners in monitoring their patients.
EPIDEMIOLOGY: AN INTRODUCTION
Although there are commonalities in the
philosophies of all scientific research, biologic
laws tend to be less universally true than are
physical laws. The set of circumstances that
leads to a heart attack in one person will not
necessarily do so in another person of the same
age, gender, and race. Biologic variation, mean-
ing the different disease susceptibility among
individuals, leads the epidemiologist to seek
patterns among people who can be grouped by
Rates
Indexes
EXAMINER RELIABILITY
MEASURING THE VALUE OF A DIAGNOSTIC
TEST
EPIDEMIOLOGY AND THE PRACTITIONER
particular characteristics. Using the characteris-
tics listed in the definition of epidemiology
given earlier, one may relate these patterns to
the following:
●
Heredity: a person’s genetic endowment
●
Biology: age, gender, race
●
Physical environment: sanitation levels, food
and water supply, air quality, occupational
hazards, housing quality, neighborhood
characteristics
●
Social environment: educational attainment,
cultural beliefs and practices, neighbor-
hood quality
●
Lifestyle: smoking, exercise, dietary pat-
terns, dental attendance, toothbrushing
habits
Heredity has received a lot of recent attention
with the rapid growth of molecular epidemiol-
ogy, that is, the application of the techniques of
molecular biology to epidemiology. DNA typ-
ing has been used to identify the genotype of
pathogenic microorganisms, and viral DNA can
be measured in host cells and their genomes.13
DNA typing can also identify the genotypes of
people who are especially susceptible to certain
diseases. Molecular epidemiology holds enor-
mous potential for disease control during the
twenty-first century.
We should remember, however, that this is
not the first time in history that there has been
great optimism about prospects for disease con-
trol. In the late nineteenth century, when the
183
184 The Methods of Oral Epidemiology
bacterial agents in many infectious diseases
were being identified, the “end of disease” was
confidently being predicted. The concept of dis-
ease at that time was dominated by acute, mor-
tal infections with a single bacterial agent, and
little thought was given to chronic conditions.
Today we are more aware that disease is multi-
factorial, meaning that multiple causative cir-
cumstances can be defined for just about any
disease. Heart disease, the leading cause of
death in the United States, is associated with
genetics, stress, diet, exercise, smoking, blood
pressure, and blood cholesterol levels. So what
is the “cause” of heart disease? Dental caries is
of bacterial origin but is also associated with
sugar consumption, fluoride exposure, saliva
quality and quantity (which are likely to be
genetically controlled), family education and
income, and other factors in the physical and
social environment. So what is the “cause” of
dental caries? Within the multifactorial tangle,
epidemiology attempts to identify the risk fac-
tors (see Chapter 13) associated with a disease
and to determine which of them are the most
important for prevention and control.
Early Studies
Epidemiology was learned and practiced empir-
ically long before it was named. For example,
people have known for ages that malaria is a
disease of wet lowlands, so they have avoided
living in such places. But there was little true
understanding about conditions that led to dis-
ease. The periodic epidemics that swept Europe
from the Middle Ages until fairly recent times,
for example, were often seen as religious signs
rather than as a result of squalid living condi-
tions. It was from the more rational study of
these epidemics that epidemiology evolved to
its present form. Samuel Pepys, who wrote vivid
chronicles of life in seventeenth-century
London, used the Bills of Mortality, the forerun-
ner of modern death certificates, to measure the
onset and decline of a plague epidemic in
London in 1665. Percivall Pott’s Treatise of the
Chimney Sweep’s Cancer, in 1775, described the
unusually high occurrence of scrotal cancer
among chimney sweeps and is thus an early sci-
entific description of an occupational hazard.
In 1854 John Snow, a medical practitioner in
the Soho area of London, went so far as to con-
trol an outbreak of cholera by the application of
his epidemiologic conclusions. His investiga-
tion took place some years before the germ the-
ory of disease was understood, so Snow began
by trying to identify the features common to
those who died from the disease. After he
mapped out the residences of those who had
died (Fig. 14-1), his subsequent inquiries dis-
closed that all of the victims had used water
from the same source. That source, in the days
before indoor plumbing, was a pump on Broad
Street (now Broadwick Street, where the site of
the pump is currently occupied by a public toi-
let). Snow reached the rational conclusion that
something in the water was responsible for the
spread of the disease. Snow’s method of con-
trolling the epidemic, still without knowing its
cause, was to persuade the authorities to remove
the pump handle. The epidemic soon subsided.
Snow’s subsequent investigations on the
relation between cholera and the source of
water supply are epidemiologic classics. The
results of the patiently executed research of
nineteenth-century workers such as Snow still
benefit present-day society. Their investigations
led to gradual but profound improvements in
sanitation and personal hygiene, and the devel-
opment of the public health codes for housing,
water supply, and food processing that are now
taken for granted. The fact that infectious dis-
eases such as cholera, typhoid, yellow fever,
plague, scarlet fever, and relapsing fever are now
rare in high-income countries is not simply
chance but is due largely to the pioneering work
of these early epidemiologists. Their work con-
tinues today: our understanding of the mode of
transmission of the human immunodeficiency
virus and its translation into public health edu-
cation to prevent acquired immunodeficiency
syndrome followed remarkably quickly on the
first identification of the virus in 1983.21,30
That, too, is epidemiology.
The types of study design used in epidemiol-
ogy were described in Chapter 13 and the vari-
ous uses of the epidemiologic method in
research are shown in Box 14-1.
The Concept of Measuring Disease
The good clinician thinks in qualitative terms.
During a diagnostic examination the dental
practitioner not only looks for existing disease
but also tries to look ahead to the possibility of
future disease. Measuring the oral health of a

Fig. 14-1 John Snow’s map of the Soho area of London, showing deaths from cholera during the epidemic of
1854.18 (From Longmate, N. Alive and well: Medicine and public health, 1830 to the present day. Hammondsworth,
Penguin, 1970.)
population, however, requires a more standard-
ized and objective approach. Specific diagnostic
criteria, written explicitly for clinical, radi-
ographic, microbiologic, or pathologic exami-
nation, provide an objective framework for the
practitioner’s judgment. These criteria are
applied to judge the condition of the oral tis-
sues as they are at examination time, not as they
might be in the future. This objective applica-
tion of diagnostic criteria is the most important
philosophical difference between the epidemi-
ologic examination and the examination car-
ried out for treatment planning.
Measurement, the quantification of observa-
tions, is the crux of science. Measurement vari-
ability is inherent in all fields of science; it is one
reason why laboratory experiments are repeated
before their findings can be accepted. In studies
of oral disease, a count of carious lesions in a
population is almost never duplicated; a repeat
14 The Measurement of Oral Disease 185
examination of the same group of patients fre-
quently results in a different count of carious
lesions. Any one count of disease in a group is
therefore an estimate of conditions, rather than
absolute truth. As long as criteria are applied
consistently, however, valid estimates will still
result, because diagnostic drifts in one direction
will be balanced by drifts the other way.
Acute diseases, such as measles, are character-
ized by a sudden onset of symptoms, so that the
patient progresses rapidly from a state in which
the disease is clearly absent to one in which the
disease is clearly present. Remission of the acute
phase of the disease is equally rapid, so little
time is spent in the “gray areas.” Chronic dis-
eases, however, are usually characterized by a
much slower onset. It is difficult to establish
exactly when arthritis, alcoholism, mental ill-
ness, dental caries, and periodontitis become
definitely established; there is a considerable
186 The Methods of Oral Epidemiology
BOX 14-1 Uses of the Science of Epidemiology
●
Describing normal biologic processes. Examples
are height at various stages of growth, blood
groups, and times and order of tooth eruption.
●
Understanding the natural history of diseases.
Observations of disease progression and outcome
in populations have enabled investigators to
distinguish those diseases that are fatal or disabling
from those that will resolve uneventfully.
●
Revealing the distribution of disease. Indicating
how disease occurs in the population by age,
gender, race, geographic region, and socioeconomic
status. Comparisons of cross-sectional surveys
conducted at different times demonstrate trends in
disease prevalence and distribution. It was the
comparison of survey results in the early 1980s
which first clearly showed that caries experience
had declined among children in the United States
(see Chapter 20).
●
Identifying the determinants of disease. Within the
multifactorial causes of disease referred to earlier,
specific study designs (see Chapter 13) can identify
the risk factors and risk indicators associated with a
disease. Even if the causal pathway of a disease is
gray area. In dentistry this problem is handled
by counting as lesions only those that meet spe-
cific criteria.
SAMPLING FROM HUMAN
POPULATIONS
Because the intent of a survey is to project results
from a sample back to the base population from
which the sample was drawn, clearly the sample
should closely represent the population.
Examples of representative sampling are
found in the national surveys of the health status
of the United States population carried out con-
tinuously by the National Center for Health
Statistics (http://www.cdc.gov/nchs). Obviously
no one project can physically examine or ask
questions of all 280 million or so Americans, so
sampling is required. The process itself is com-
plicated and requires specialized training, but
sampling precision is such that the 100,618 per-
sons interviewed in the 2000 National Health
Interview Survey28 could represent the whole
not fully understood, knowledge of risk factors can
lead to intervention strategies for prevention and
control.
●
Testing hypotheses for disease prevention and
control. Agents, regimens, or procedures for the
prevention and control of disease can be
experimentally tested in clinical trials (see Chapter
13). As a dental example, the various uses of
fluorides to reduce caries incidence have been
subjected to numerous field trials in human
populations (see Chapters 25 and 26).
●
Planning and evaluating health care services.
Data that describe (1) the distribution of disease,
both treated and untreated, in the population
under study; (2) the population’s utilization
of health care services; and (3) the availability
and productivity of health care services can be
employed to assist planning decisions on
services and types of personnel required.
Related applications are validation of the
effectiveness of treatment techniques, both new
and traditional, and determination of the quality
of treatment provided.
country with a low degree of sampling error.
Sampling error is the discrepancy between the
sample and the base population in one or more
important characteristics, and with modern sta-
tistical methods it can be remarkably small. The
type of sample used in the National Health
Interview Survey is a probability sample, which
means that the chance of each person’s being
selected in the sample is known, though not
necessarily equal. A greater proportion of older
people than younger people, for example, may
be deliberately sampled to compensate for the
poorer response that is characteristic of older
people. What is important is that the sampling
probability be known, because then the degree of
sampling error can be calculated.
When a nonprobability sample is used for a
survey, however, interpretive problems arise
because sampling error cannot be calculated
from nonprobability samples. As an example,
the National Survey of Oral Health in U.S.
Employed Adults and Seniors in 1985-8629
sought to obtain a profile of oral health in

American adults by examining employed adults
and seniors who visited senior centers. This was
a practical and budget-conscious way of obtain-
ing a reasonable profile, but the restricted sam-
pling most likely introduced bias into the
results. For example, the survey found that only
4.2% of persons under age 65 were edentulous,
but this is almost certainly an underestimate
because various groups (e.g., the unemployed
and self-employed) were excluded from the
sampling frame, which means that they had no
chance of selection in the sample.
Note that analytic studies in epidemiology
usually do not use probability samples. In fact,
case-control and cohort studies, as well as clini-
cal trials (see Chapter 13), are usually conducted
with groups carefully chosen for required attrib-
utes such as age, accessibility, presence of both
the disease and the exposures under study, and
willingness to participate. In analytic study
designs, a prime critical issue is the selection and
categorization of participants as cases or con-
trols, or exposed and unexposed. In clinical tri-
als, the prime critical issue is the allocation of
participants to test or control group.
More than one analytic study is usually
required before the identification of a risk factor
can be confirmed or the results of a clinical
trial can be generalized. If weekly use of a
fluoride mouthrinse is found to reduce
caries incidence by 22% over 30 months among
12-year-old children in fluoridated Des
Moines,6 what does that mean for the children
of the United States as a whole? Even assuming
experimental conditions could be identical
(which they never are), results need not neces-
sarily be the same for children of different eth-
nic backgrounds, living in different climatic
zones, and with differing dietary practices and
exposure to fluoridated water. When additional
studies are carried out by different researchers in
different places with fairly similar results, how-
ever, then the weight of evidence increases the
likelihood that the observed effect is real and
generalizable to the population at large.
METHODS OF MEASURING ORAL
DISEASES
Counts
The simplest way of measuring any disease is by
counting the number of cases of its occurrence.
14 The Measurement of Oral Disease 187
Simple counts of cases are most useful for
unusual conditions of low prevalence (e.g., the
130 or so incident cases of Ewing’s tumor in
children under 15 years of age in the United
States each year). Simple counts become less
useful as prevalence increases.
Proportions
A count becomes a proportion when a denomi-
nator is added, and prevalence is thus deter-
mined. The count of cancers in males ages
55-64 years can be divided by the population of
that group to give prevalence: 22 cases in a pop-
ulation of 845 men ages 55-64 years yields a
prevalence of 0.026, or 2.6%. Proportions do
not include a time dimension; the figure just
given would include newly diagnosed cases as
well as longstanding ones. Proportions can also
be useful in expressing the prevalence of caries
among schoolchildren, the prevalence of total
tooth loss in adults, or the prevalence of other
conditions whose occurrence is somewhere
between common and rare.
Rates
A rate is a proportion that uses a standardized
denominator and includes a time dimension.
Infant mortality rate, for example, is the num-
ber of deaths of newborn infants within the first
year of life per 1000 live births, usually stated
for particular calendar years to illustrate trends.
In the United States the infant mortality rate for
white children dropped from 6.3 per 1000 live
births in 1995 to 5.7 in 2001; for African-
American children the same measures were
14.6 and 13.3.28
Rates have not been used much in oral dis-
ease measurement, except to describe caries
incidence over a period of time in clinical trials6
and annual rate of loss of periodontal attach-
ment in longitudinal studies.17 Proportions or
index values are often mistakenly referred to as
rates in the literature.
Indexes
The individual who suffers from caries in only
2 of 32 teeth clearly has a much lower intensity
of disease than does the person who has carious
lesions in 16 of 26 teeth. Simple prevalence
does not discriminate between these degrees of
intensity, which is usually determined in oral
epidemiology by use of an index (the plural
188 The Methods of Oral Epidemiology
BOX 14-2 Properties of an Ideal Index
●
Validity. The index must measure what it is
intended to measure, so it should correspond with
the clinical stages of the disease under study at each
point.
●
Reliability. The index should be able to measure
consistently at different times and under a variety of
conditions. The term reliability is virtually
synonymous with reproducibility, repeatability, and
consistency, meaning the ability of the same or
different examiners to interpret and use the index in
the same way.
●
Clarity, simplicity, and objectivity. The criteria
should be clear and unambiguous, with mutually
form we will use is indexes, although indices is
also used).
An index is a numerical scale with upper and
lower limits, with scores on the scale correspon-
ding to specific criteria. Index scores can be
expressed for an individual; populations can
be characterized by distributions or mean scores.
The properties of an ideal index are listed in Box
14-2. Index scores frequently are clinical abstrac-
tions (e.g., a Plaque Index score of 1.2), which
only make sense when used for comparisons
between individuals or groups measured in a
similar way. In the literature, the word index is
often used broadly to mean any form of disease
quantification, including proportions and rates.
We encourage confining its use to scales meeting
the aforementioned definition. The criteria for
assigning a particular score to a condition are an
integral part of the description of any index.
The different types of scales used in disease
measurement are shown in Box 14-3. The
majority of indexes used in oral epidemiology
are ordinal scales, although some are treated
statistically as though they were interval or ratio
scales. This statistical impropriety can be a bit
academic, however, because such deviations
usually do not give seriously misleading results.
There are other terms used in the literature to
describe indexes, such as reversible and irre-
versible. An irreversible index is one that meas-
ures cumulative conditions that cannot be
reversed: dental caries (e.g., caries that has
resulted in tissue loss, either restored or unre-
exclusive categories. Ideally, they should be able to
be readily memorized by an examiner after some
practice.
●
Quantifiability. The index must be amenable to
statistical analysis, so that the status of a group can
be expressed by a distribution, mean, median, or
other statistical measure.
●
Sensitivity. The index should be able to detect
reasonably small shifts, in either direction, in the
condition.
●
Acceptability. The use of the index should not be
painful or demeaning to the subject.
BOX 14-3 Types of Scale Used in Disease
Measurement
●
Nominal. A scale that simply gives names to
different conditions and therefore is not strictly a
scale at all, e.g., Angle’s classification of
malocclusions.3
●
Ordinal. A scale that lists conditions in some order
of severity without attempting to define any
mathematical relation between the categories, e.g.,
the Gingival Index of Löe and Silness.17
●
Interval. A scale in which the numbers used in the
scale purport to have a mathematical relation to
each other, although the scale does not have a true
zero point. Examples are the Fahrenheit and Celsius
temperature scales; none known in dentistry.
●
Ratio. A scale in which the numbers used in the
scale purport to have a mathematical relation to
each other, and the scale has a true zero point. An
example is the Kelvin temperature scale, which goes
to absolute zero. A dental example, though one no
longer in use (see Chapter 16) is the Russell
Periodontal Index.27
stored, or tooth loss itself). However, gingivitis
is a reversible inflammatory condition, so an
index of gingivitis is considered reversible.
A final general point about disease measure-
ment is that, just as there is no perfect method,
there are also no generic, all-purpose scales that
meet every need. Choice of measurement scale

in any situation, whether it be for a practitioner
monitoring a patient’s progress or for a
researcher conducting a highly sophisticated
clinical trial, is dictated by the needs. The first
response to the often-asked question of “What
index should I use?” is “What is the question you
want to answer?” The process a practitioner goes
through to select a measure by which to monitor
the oral hygiene progress of a middle-aged peri-
odontal patient is little different from that fol-
lowed by the researcher in a complex study. Both
have to determine why they are using that partic-
ular measure, how to handle it reliably, and
what it is they want to demonstrate.
EXAMINER RELIABILITY
When any measurements of disease are made
over a period of time, conclusions reached are
based on the comparison between two sets of
results. It follows that the diagnostic criteria
must be applied the same way at different times,
because if they are not, the comparisons have lit-
tle value. This is the issue of examiner reliability,
which was introduced in Chapter 13. Assuming
that the index is inherently reproducible, the
ability of an examiner to record the same condi-
tions the same way over time is termed intraex-
aminer reliability. This quality can be developed
by most examiners with some training and
experience, but it needs to be demonstrated in
research studies. Intraexaminer reliability can be
assessed by having an examiner record condi-
tions in a group of 10-20 persons and then
repeat the process a few hours to a few days later.
The time between the first and second examina-
tions should be long enough for memory to fade
but short enough so that real change in the
condition itself will not be noticeable. Reaching
agreement between two or more examiners,
interexaminer reliability, is usually more tedious.
It requires initial agreement on interpretation
of diagnostic criteria, then a period of training
with repeated patient examinations to ensure
that examiners’ judgments are comparable.
Interexaminer reliability is rarely perfect, but
when examination findings from two or more
examiners are being pooled, a measure of
interexaminer reliability training should be
recorded. This conforms with the CONSORT
(Consolidated Standards of Reporting Trials)
Statement, a set of criteria for explicit reporting of
14 The Measurement of Oral Disease 189
clinical trials (see Chapter 12), which lists “any
methods used to enhance quality of measure-
ments” as one of the elements to be reported.19
The issue of examiner reliability can make
people uncomfortable, because to have one’s
inconsistencies exposed for the world to see can
be humbling. (We stress that examiner reliabil-
ity is totally unrelated to clinical skills or ability
to care for patients.) In the literature, examiner
reliability is sometimes vaguely dismissed with
a statement like “the examiners achieved 96%
agreement,” which by itself is of little value
because of its uncertain meaning (it usually
seems to mean that one examiner’s group mean
score was 96% of the mean score of the other
examiner’s group). In addition, such a compari-
son does not account for decisions requiring lit-
tle diagnostic judgment (e.g., inclusion of many
obviously sound lower incisors in the denomi-
nator), nor does it account for agreement that
would be expected by chance alone.10 The meas-
ure most frequently used for expressing interex-
aminer reliability is the kappa statistic, a value
between 0 and 1.0 that expresses the degree of
agreement beyond that expected by chance
alone.10,12 Correlation statistics and specified
percent agreement, along with kappa, give a
good picture of interexaminer reliability in a
cross-sectional study.
Reversals can be exasperating in longitudinal
studies, notably in clinical trials. A reversal, more
properly called a negative reversal, is a change of
diagnosis in an illogical direction over a period
of time long enough for real change to have
taken place. For example, when a surface scored
as caries into dentin at the first examination is
scored as sound 1 year later, this is an illogical
change. In a clinical trial, the examiner has to
record disease that developed over a relatively
short time; hence, much of it is at incipient
stages. Diagnosis of borderline lesions as caries
inevitably results in some degree of negative
reversals, so reversals are an inherent part of any
clinical trial.25 What must be remembered about
reversals, however, is that if the examiner is con-
sistent then negative reversals will be balanced
by positive reversals, which are changes in a logi-
cal direction made in error. In a caries trial this
means that a lesion diagnosed as sound at the
first examination is marked as carious a year
later, when the diagnosis really should have
been sound-sound or carious-carious. The snag,
190 The Methods of Oral Epidemiology
of course, is that at data analysis the positive
reversals cannot be separated from normal dis-
ease progression. That is where a demonstration
of reliability is important: even if the examina-
tions are all of incipient lesions in first molars,
where many reversals would be expected, a con-
sistent examiner will have negative reversals bal-
anced by positive reversals. Net results should
therefore be analyzed without subtracting out
the negative reversals.
Reversals are illustrated in Fig. 14-2, which
uses 10 tooth surfaces being measured for caries
to illustrate the point. Surfaces A to C have pro-
gressed from sound to decayed, but D and E
(shaded) show negative reversals. The remaining
teeth have not changed in diagnosis between
examinations. The net result is that the four D
lesions at baseline have become five lesions a
year later. But how is this analysis affected by the
negative reversals in D and E? Reversals at best
can be disturbing (indeed, if the reliability exam-
inations cast doubt on the examiner’s reliability,
then the entire set of data is suspect). If, however,
the examiner is acceptably consistent, then it can
be assumed that the two negative reversals in D
and E are random errors and will be balanced by
two positive reversals in A, B, or C. There could
also have been random error in the diagnoses for
surfaces F to J, but because all these diagnoses are
in a logical direction, such error cannot be
Fig. 14-2 Representation of positive and neg-
ative diagnostic reversals in a longitudinal study.
detected. The net result of four decayed lesions
progressing to five therefore is retained and
referred to as the net caries increment.
Reversals in longitudinal studies of periodon-
titis are especially troublesome because reattach-
ment has been demonstrated by experienced
examiners.15 A loss of periodontal attachment of
6 mm at initial examination that is then recorded
as 5 mm a year later could represent examiner
error or it could be true reattachment. A demon-
stration of examiner reliability in diagnosis is
especially important in these circumstances.
Reliability in periodontal examinations has been
improved with the advent of pressure-sensitive
and computerized probes,11,24 although the use
of these instruments is largely restricted to clini-
cal research studies.
Note the difference between an examination
to check reliability and the occurrence of rever-
sals. A reliability check consists of repeat exami-
nations only hours apart, too close together
for real change to have occurred. Differences in
diagnosis are therefore all examiner variation.
Reversals occur over a period of time long
enough for real change to have occurred, so
examiner variation can be mixed in with real
change. In a reliability check, the duplicate
examinations do not form a part of the data set,
whereas reversals are detected from the study
data.
 14 The Measurement of Oral Disease 191

or other biologic tests that could predict caries

MEASURING THE VALUE
OF A DIAGNOSTIC TEST
We discussed in Chapters 12 and 13 that the
ultimate test for the efficacy of a preventive
agent or procedure was the randomized clinical
trial, but this design does not fit when the pur-
pose is evaluation of a diagnostic test.
Diagnostic tests in medicine are numerous
and well established. The criteria for an ideal
test are that it should be simple, inexpensive
(relative to the direct or social cost of the dis-
ease), acceptable to the patient, valid, and reli-
able. A test should also be sensitive, which in this
context means that it yields a positive result in
those with the disease, and specific, meaning
that it gives a negative result in those who do
not have the disease. There are only a few tests
that rate highly in both sensitivity and speci-
ficity, so the choice may be whether to use a test
that is highly sensitive but not very specific
(which would capture a lot of false positives—
people who test positive but really don’t have
the disease), specific but not sensitive (which
would lead to a lot of false negatives—people
who test negative but really do have the dis-
ease), or not to test at all. Fig. 14-3 summarizes
how sensitivity, specificity, and related predic-
tive values can be derived from the results of
tests and subsequent disease outcome.
In dentistry a considerable number of predic-
tive tests intended to identify caries-susceptible
individuals have been explored down the years
without much success. A 1977 conference at
Niagara Falls concluded that there was little at
that time in the way of bacteriologic, enzymatic,
with sufficient sensitivity and specificity. The
best predictor of future caries was past caries
experience,5 a result that is consistently found
in more recent studies as well.9,14,26 This find-
ing is not much help to a practitioner trying to
control caries in a susceptible patient.
Research aimed at finding tests for suscep-
tibility to severe periodontitis still has some
way to go.1,22 The only true risk factors estab-
lished are tobacco use and diabetes,1 although
inflammatory mediators identified in gingival
crevicular fluid may in time form the basis of
practical tests of susceptibility.2 Clinical signs
such as gingivitis, plaque deposits, suppuration,
and bleeding on probing have demonstrated
poor sensitivity, and even a pocket depth of 4
mm or more is only weakly predictive at best for
severe periodontitis.8,20 There has been some
modest progress in exploring risk factors in the
physical and social environment such as stress
and anxiety, income level, and poor ability to
cope with life’s pressures.4,7 Although many of
these factors, apart from smoking and diabetes,
have not yet been unequivocally related to peri-
odontitis, some have been put together into a
“risk calculator” that is reasonably valid.23
Further refinements in this area can be expected.
EPIDEMIOLOGY
AND THE PRACTITIONER
Epidemiology joins the basic sciences and clini-
cal studies to increase our understanding of dis-
eases. The practitioner can factor knowledge
of risk factors into diagnosis and treatment

Test result Disease No disease Total

Positive TP FP TP + FP
Negative FN TN TN + FN
Total TP + FN FP + TN ALL
Sensitivity: Proportion of people with disease who test positive: TP/(TP + FN)
Specificity: Proportion of people without disease who test negative: TN/(FP + TN)
Positive predictive value: Probability that a person who tests positive will have disease: TP/(TP + FP)
Negative predictive value: Probability that a person who tests negative will not have disease: TN/(FN + TN)
False-positive rate: Proportion of people with positive tests who do not have disease: FP/(FP + TN)
False-negative rate: Proportion of people with negative tests who have disease: FN/(TP + FN)

Fig. 14-3 Information that can be derived from the results of a predictive test related to disease outcome. TP, True
positive; TN, true negative; FP, false positive; FN, false negative.
192 The Methods of Oral Epidemiology
planning decisions; that is, a patient is more
likely to develop a particular disease if he or she
exhibits certain characteristics. For example, a
man who smokes may or may not get lung can-
cer, but he certainly runs more risk of develop-
ing lung cancer than if he did not smoke.
Similarly, an elderly man who both smokes and
drinks heavily is more at risk of oral cancer than
one who does not.
Another immediate use of epidemiology to
the practitioner is application of the results from
clinical trials, preferably from systematic reviews,
which form the cornerstone of evidence-based
dentistry (see Chapter 12). Although not every
member of a test group in a clinical trial necessar-
ily benefits from the tested procedure, the proba-
bilities are high that a given patient will benefit
from a procedure that has been successfully
tested.
Biologic variation also applies the other way:
a practitioner cannot generalize from the results
of an individual patient’s treatment to the pop-
ulation at large. Successful treatment can result
from a practitioner’s personality, from serendip-
itous characteristics of the particular patient, or
from outside influences, as well as from the
treatment itself. Clinical experience is impor-
tant, but only with controls and the appropriate
design can effective prevention and treatment
methods be clearly identified.
REFERENCES
1. Albandar JM. Global risk factors and risks indicators
for periodontal disease. Periodontol 2000; 2002;29:
177-206.
2. Alpagot T, Bell C, Lundergan W, et al. Longitudinal evalu-
ation of GCF MMP-3 and TIMP-1 levels as prognostic fac-
tors for progression of periodontitis. J Clin Periodontol
2001;28:353-9.
3. Angle EH. Classification of malocclusion. Dent Cosmos
1899;41:248-64.
4. Beck JD, Koch GG, Offenbacher S. Incidence of attach-
ment loss over 3 years in older adults—new and pro-
gressing lesions. Community Dent Oral Epidemiol
1995;23:291-6.
5. Bibby BG, Shern RJ, eds. Methods of caries prediction;
proceedings of a workshop conference. Washington
DC: Information Retrieval, 1978.
6. Driscoll WS, Swango PA, Horowitz AM, Kingman
A. Caries-preventive effects of daily and weekly fluoride
mouthrinsing in a fluoridated community: Final results
after 30 months. J Am Dent Assoc 1982;105:1010-3.
7. Genco RJ, Ho AW, Grossi SG, et al. Relationship of
stress, distress, and inadequate coping behaviors to
periodontal disease. J Periodontol 1999;70:711-23.
8. Haffajee AD, Socransky SS, Goodson JM. Clinical
parameters as predictors of destructive disease activity.
J Clin Periodontol 1983;10:257-65.
9. Hausen H, Seppä L, Fejerskov O. Can caries be pre-
dicted? In: Thylstrup A, Fejerskov O, eds: Textbook of
clinical cariology. 2nd ed. Copenhagen: Munksgaard,
1994:393-411.
10. Hunt RJ. Percent agreement, Pearson’s correlation, and
kappa as measures of inter-examiner reliability. J Dent
Res 1986;65:128-30.
11. Jeffcoat MK, Jeffcoat RL, Jens SC, Captain K. A new peri-
odontal probe with automated cemento-enamel junc-
tion detection. J Clin Periodontol 1986;13:276-80.
12. Landis JR, Koch GG. The measurement of observer
agreement for categorical data. Biometrics 1977;33:
159-74.
13. Last JM. A dictionary of epidemiology. 3rd ed. New
York: OUP, 1995.
14. Leverett DH, Proskin HM, Featherstone JD, et al. Caries
risk assessment in a longitudinal discrimination study.
J Dent Res 1993;72:538-43.
15. Lindhe J, Haffajee AD, Socransky SS. Progression of peri-
odontal disease in adult subjects in the absence of peri-
odontal therapy. J Clin Periodontol 1983;10:433-42.
16. Löe H, Ånerud A, Boysen H, Morrison E. Natural his-
tory of periodontal disease in man. Rapid, moderate
and no loss of attachment in Sri Lankan laborers 14 to
46 years of age. J Clin Periodontol 1986;13:431-40.
17. Löe H, Silness J. Periodontal disease in pregnancy.
I. Prevalence and severity. Acta Odontol Scand 1963;21:
533-51.
18. Longmate N. Alive and well: Medicine and public
health from 1830 to the present day. Harmondsworth
UK: Penguin, 1970.
19. Moher D, Schultz KF, Altman DG, for the CONSORT
group. Revised recommendations for improving the
quality of reports of parallel group randomized trials
2001, website: http://www.consort-statement.org/.
Accessed November 20, 2003.
20. Norderyd O, Hugoson A, Grusovin G. Risk of severe
periodontal disease in a Swedish adult population.
A longitudinal study. J Clin Periodontol 1999;26:
608-15.
21. Osborn JE. Dispelling myths about the AIDS epidemic.
In: Fransen VE, ed: Proceedings of the AIDS prevention
and services workshop. Princeton NJ: Robert Wood
Johnson Foundation, 1990:15-21.
22. Page RC, Beck JD. Risk assessment for periodontal dis-
eases. Int Dent J 1997;47:61-87.
23. Page RC, Krall EA, Martin J, et al. Validity and accuracy
of a risk calculator in predicting periodontal disease.
J Am Dent Assoc 2002;133:569-76.
24. Polson AM, Goodson JM. Periodontal diagnosis; current
status and future needs. J Periodontol 1985;56:25-34.
25. Radike AW. Examiner error and reversals in diagnosis.
In: Proceedings of the conference on the clinical testing
of cariostatic agents. Chicago: American Dental
Association, 1972:92-5.
26. Reich E, Lussi A, Newbrun E. Caries risk assessment. Int
Dent J 1999;49:15-26.
27. Russell AL. A system of scoring for prevalence surveys of
periodontal disease. J Dent Res 1956;35:350-9.

28. US Public Health Service, National Center for
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29. US Public Health Service, National Institute of Dental
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Public Health 1988;78:364-6.
 15 Measuring Dental Caries
DMF INDEX
CRITERIA FOR DIAGNOSING CORONAL
CARIES
This chapter describes the methods for measur-
ing dental caries in human populations. Some
historical measures from the early twentieth
century include the proportion of first molars
lost through caries21,22 and the percentage of
erupted permanent teeth affected by caries.1
Both of these measures were useful when there
was little information of any kind about the dis-
ease, though they lacked sensitivity. At the other
extreme, the Bodeckers’ index of surfaces
affected by caries, described in 1931,10 was sen-
sitive but complicated. Dean and his col-
leagues,14 in their pioneering studies of the
caries-fluoride relationship, counted the num-
ber of teeth in the mouth visibly affected by
caries, which was a forerunner of the DMF
count. The first description of what is now
known as the DMF index is attributed to Klein,
Palmer, and Knutson in their studies of dental
caries in Hagerstown, Maryland, in the 1930s.32
Since then, the DMF index has received practi-
cally universal acceptance and is the best known
and most widely used of all dental indexes.
DMF INDEX
The DMF index, an irreversible index, is applied
only to permanent teeth. As originally described,
it defined three categories of teeth that were
counted to calculate the index:
D for decayed teeth
M for teeth missing due to caries
F for teeth that had been previously filled
Filled teeth were assumed to have been
unequivocally decayed prior to restoration. The
DMF score for any one individual can range from
194
ROOT CARIES
EARLY CHILDHOOD CARIES
CARIES TREATMENT NEEDS
0 to 32, in whole numbers. A mean DMF score
for a group, which is the total of individual val-
ues divided by the number of subjects examined,
can have a decimal value. The DMF index can be
applied to whole teeth (designated as DMFT) or
to surfaces (DMFS). Modifications can be made
to the index for factors such as filled teeth that
have redecayed, crowned teeth, bridge pontics,
and any other particular attribute required for a
given study. To save time in a large survey, the
DMF index can be used half-mouth; that is, it can
be applied to opposite diagonal quadrants and
the score doubled, an approach which assumes
that the carious attack is bilateral. The DMF index
can be applied to all 32 teeth, although because
of the widespread removal of third molars in
young adults some prefer to record a score for 28
teeth. Either approach is acceptable as long as the
method is clearly stated.
Although the DMF index has been used uni-
versally since its introduction in 1938, its limi-
tations need to be recognized. The main ones
are shown in Box 15-1.
The DMF index for permanent teeth is always
signified by uppercase letters; the equivalent
index for the primary dentition is the def index
and its modifications.19 The teeth counted to
derive this index were originally defined as
follows:
d for decayed teeth
e for teeth indicated for extraction
f for filled teeth.
Teeth missing because of caries are not
recorded because of the complications of exfoli-
ation and lack of knowledge as to whether miss-
ing teeth were carious prior to exfoliation.

BOX 15-1 Limitations of the DMF Index
The DMF index has received remarkably little
challenge over some 70 years of life, probably because
it is simple and versatile. It was developed for use in
children a long time ago, however, and accordingly it
shows its age in a few areas. The principal limitations
are the following:
●
DMF values are not related to the number of teeth at
risk. A DMF score for an individual is a simple count
of those teeth that in the examiner’s judgment have
been affected by caries; it has no denominator.
A DMF score thus does not directly give an indication
of the intensity of the attack in any one individual.
A 7-year-old child with a DMF score of 3.0 may have
only 9 permanent teeth in the mouth; thus one third
of these teeth have already been attacked by caries in
a short space of time. An adult may have a DMF
score of 8.0 with a full complement of 32 teeth; thus
over a longer period of time only one quarter of the
teeth have been affected. DMF scores therefore have
little meaning unless age is also stated.
●
The DMF index gives equal weight to missing,
untreated decayed, and well-restored teeth.
Common sense suggests that this philosophical
basis is faulty for many purposes.
Modifications of this index are (1) the dmf
index for use in children before the age of exfo-
liation, (2) the dmf index applied only to the
primary molar teeth, and (3) the df index.
Values for df and def should be numerically the
same; def allows for two grades of caries, and
neither index counts missing teeth. Both the def
and df indexes may therefore understate the
true extent of the carious attack; the trade-off is
presumably greater reliability from ignoring
missing teeth.
Because of the present-day skewed distribu-
tion of caries prevalence in the population, the
Significant Caries Index (SiC Index) was devel-
oped.11 The SiC Index is not a new index,
because it is based on the distribution of DMF
values in a population, but is a way of express-
ing caries distribution that goes beyond mean
DMF. It is actually the mean DMF score for the
third of the distribution most affected by caries
and is intended to be used alongside the mean
DMF value to give a more complete summary of
caries in the whole population. The more
15 Measuring Dental Caries 195
●
The DMF index is invalid when teeth have been lost for
reasons other than caries. Teeth can be lost for
periodontal reasons in older adults and for
orthodontic reasons in teenagers. Decision rules,
which go along with criteria, are required to determine
how to deal with these instances.
●
The DMF index can overestimate caries experience in
teeth with “preventive restorations.” In an
epidemiologic survey, such teeth must be included in
the F component of DMF, although had they not been
filled in the first place they might have been diagnosed
as sound teeth. DMF scores will thus be inflated.5
Composite restorations judged to have been placed
only for cosmetic reasons likewise should not be
included in DMF counts.
●
DMF data are of little use for estimating treatment
needs (see Caries Treatment Needs).
●
The DMF index cannot account for sealed teeth.
Sealants did not exist in 1938 and thus are obviously
not included in the description of the index. Here is
where the DMF index shows its age; sealants and
other composite restorations for cosmetic purposes
have to be dealt with separately.
skewed the distribution, the greater the gap
between the mean DMF score and the SiC value.
A new global goal of an SiC score of 3.0 or less
for 2015 has been suggested57 and, if adopted
and used, would provide some further informa-
tion on caries distribution.38
Other methods of measuring dental caries
with a different philosophical base have been
suggested. One is Grainger’s hierarchy, an ordi-
nal scale designed to simplify the recording of
the caries status of a population, which uses five
zones of severity of the carious attack.18 This
scale appears to be valid29,31,45 but has received
little further use, probably because of low sensi-
tivity. More recently, “composite” indicators
have been suggested that attempt to measure
health rather than disease by weighting healthy
restored teeth differently from missing or
decayed teeth.46 The first of these is the FS-T,
which sums the sound and healthy restored
teeth. The second is T-Health, which seeks to
measure the amount of healthy dental tissue
and assigns descending numerical weights for a
196 The Methods of Oral Epidemiology
sound healthy tooth, a filled tooth, and a
decayed tooth. These are conceptually sound
approaches to measuring dental health and
function (rather than disease), and they deserve
more attention than they have received.
Sealants had not arrived when the DMF
index first appeared, but there are two reason-
able approaches for dealing with sealants in the
DMF system. One view holds that the sealed
tooth is not restored in the classic sense and
should therefore be considered sound. The
other contends that it has required hands-on,
one-to-one dental attention and so should be
considered a filled tooth. Probably the best way
to deal with sealed teeth is to put them into a
category by themselves, S for sealed. The DMFS
index would then become DMFSS. Depending
on the purpose of a given study, the S teeth can
be left separate, included with the F teeth, or
regarded as sound.
With modern preventive and restorative
technology, the DMF index is really outdated as
a measure of caries attack; the index may be
more valid as a measure of treatment received. It
is philosophically questionable to use a disease
index that is so dependent on the treatment
judgments of many practitioners, and combin-
ing previous treatment (i.e., the M and F com-
ponents) with current treatment need (the D
component) is unsuitable for surveillance pur-
poses (see Chapter 4). A measure of caries activ-
ity would be preferable for many purposes, but
approaches to scoring caries activity are still
based on clinical acumen.41 Until a more objec-
tive measure is developed and accepted, the
DMF index will continue to be used. The results
of its use, however, should always be interpreted
with care.
CRITERIA FOR DIAGNOSING
CORONAL CARIES
There is no global consensus on the criteria for
diagnosing dental caries, despite a vast quantity
of words on the subject. Different traditions
about defining a lesion in the gray area, where it
is difficult to tell whether the disease is irre-
versibly established or not, have grown up and
are still adhered to. Apart from the inherent
problem of diagnosing a borderline lesion, the
major philosophical issue is how to score an
early carious lesion that has not yet become cav-
itated, whether diagnosed clinically or radi-
ographically. Such a lesion appears as a discol-
ored fissure without loss of substance, as a
“white spot” on visible smooth surfaces, or
radiographically as an early interproximal
shadow. The issue is that not all noncavitated
lesions progress to become dentinal lesions
requiring restorative treatment; a good propor-
tion of them remain static or even remineralize,
especially smooth surface lesions.43 These
lesions are thus reversible, as opposed to a
dentinal lesion, which is generally considered
irreversible. Because there are usually more
noncavitated than cavitated lesions at any
one time in both high-caries and low-caries
populations,9,23,44 the decision as to whether to
include or exclude them, and how to express
them if included, can make a substantial
difference in the oral health profiles obtained.
Examples of these two different approaches
to diagnostic criteria for dental caries are shown
in Box 15-2. Traditionally, European investiga-
tors have recorded caries on a scale that extends
through the full range of disease from the earli-
est detectable noncavitated lesion through to
pulpal involvement.3 The criteria in Box 15-2
are based on those first published by the World
Health Organization (WHO) in 197954 and
now usually referred to as the D1-D3 scale.
Clinical researchers in Europe have expanded
on this concept to produce a scale with up to 10
points, combining increasing depths of lesion
development with clinical signs of activity or
inactivity.37 On the other hand, investigators in
North America, Britain, and the other English-
speaking countries have traditionally recorded
caries as a dichotomous condition, meaning
that caries is diagnosed only as present or
absent. (We refer to this as the dichotomous
scale.) In dichotomous recording, caries is only
noted when it has reached the level of dentinal
involvement,20 that is, the D3 level. Use of the
D1-D3 scale requires that the teeth be dried and
be given a longer, more meticulous survey
examination. Although there are more diagnos-
tic decisions to make when the D1-D3 scale is
used, adequate examiner reliability can be
maintained when examiners have been trained
in this system.43
The D1-D3 scale is extremely valuable in
research studies on dental caries, because it per-
mits identification of lesion progression as well

BOX 15-2 Criteria for Diagnosis of Caries Through the Full Range of Lesion Development (D1-D3 Scale)
Compared With Criteria for Diagnosis at the Dentinal Lesion Stage Only (Dichotomous Scale)20,44,55
Diagnosis through the Full Range of Caries:
the D1-D3 scale
0. Surface sound. No evidence of treated or
untreated clinical caries (slight staining allowed in an
otherwise sound fissure).
D1. Initial caries. No clinically detectable loss of
substance. For pits and fissures, there may be
significant staining, discoloration, or rough spots in
the enamel that do not catch the explorer, but loss of
substance cannot be positively diagnosed. For smooth
surfaces, these may be white, opaque areas with loss
of luster.
D2. Enamel caries. Demonstrable loss of tooth
substance in pits, fissures, or on smooth surfaces, but
no softened floor or wall or undermined enamel. The
texture of the material within the cavity may be chalky
or crumbly, but there is no evidence that cavitation has
penetrated the dentin.
D3. Caries of dentin. Detectably softened floor,
undermined enamel, or a softened wall, or the tooth
has a temporary filling. On approximal surfaces, the
explorer point must enter a lesion with certainty.
*The area should be diagnosed as sound when there is apparent evidence of demineralization but no evidence of softness.
as initiation. Research questions on the condi-
tions under which early lesions progress,
regress, or remain static can thus be answered
only with the use of such a measurement scale.
Its application demands meticulous examiner
training because D1 lesions are capable of rem-
ineralizing back to sound enamel, and it thus
becomes difficult to differentiate examiner error
from natural phenomena. There is less consen-
sus on whether the D1-D3 scale should be used
in large-scale surveys, and there are no examples
of this having been done. Arguments can be
made both ways, but on balance we believe that
more benefit is to be gained if surveys continue
to diagnose caries at the D3 level only, that is,
using the dichotomous scale.12
Caries diagnosis by clinical means, irrespec-
tive of the criteria adopted, has traditionally used
visual-tactile methods; that is, it has used the
explorer as well as vision. Indeed, the criteria
listed in the dichotomous scale in Box 15-2
explicitly require use of the explorer. Our current
understanding of caries, however, indicates that
15 Measuring Dental Caries 197
D4. Pulpal involvement. Deep cavity with probable
pulpal involvement. Pulp should not be probed.
(Usually included with D3 in data analysis.)
Diagnosis at the Dentinal Lesion Stage Only:
the Dichotomous Scale
Pits and fissures on the occlusal, vestibular, and
lingual surfaces are carious when the explorer
“catches” after insertion with moderate to firm
pressure and when the “catch” is accompanied by one
or more of the following signs of decay:
1. Softness at the base of the area.
2. Opacity adjacent to the area* providing evidence of
undermining or demineralization.
3. Softened enamel adjacent to the area that may be
scraped away by the explorer.
routine use of the explorer in this way is likely to
damage the enamel matrix of noncavitated
lesions where remineralization is taking place. As
a result, European criteria for diagnosing caries
in the 1990s have moved toward exclusively
visual criteria.42 Initial studies with a group of
dentists using extracted teeth that later were sec-
tioned and histologically examined found that
use of the explorer did not add to the value of
visual diagnosis.34,35 The series of surveys for
monitoring caries in British children that is car-
ried out by the British Association for the Study
of Community Dentistry, really a surveillance
system, uses the exclusively visual approach in
its protocol. Caries is recorded at the D3 level,
and the criterion for caries is the following: “if, in
the opinion of a trained examiner, after visual
inspection there is a carious lesion into dentine,”
then caries is recorded.43 Use of this criterion
requires extensive examiner training and meticu-
lous drying of the teeth. The third National
Health and Nutrition Examination Survey
(NHANES III) in the United States, 1988-94,
198 The Methods of Oral Epidemiology
retained the traditional dichotomous criteria
shown in Box 15-2.25
Caries diagnosis is also complicated by hidden
caries, the name given to dentinal caries found
radiographically beneath an apparently sound
occlusal surface.30,43,52 This condition is poorly
understood, although it is hardly rare; studies
found hidden caries in 7.5% of a group of Dutch
children53 and 2%-5% of Lithuanian children.37
Some see it as a by-product of the fluoride age, in
which the original break in the enamel reminer-
alizes before the dentinal lesion has reached the
pulp, but its natural history is really unknown.
Additional research on this condition is clearly
needed. The possibility of hidden caries has led
to a further look at the use of radiographs for
caries diagnosis at a time when they generally
are not employed in caries epidemiologic stud-
ies and clinical trials for ethical reasons (unnec-
essary radiation exposure when not used in the
course of treatment), costs, and the risk of bias
that comes from the refusal of some study par-
ticipants to undergo radiography.
Newer methods of caries diagnosis, such as
fiberoptic transillumination, electrical conduc-
tance, and laser fluorescence, have shown
promise2,30,36 and may find a role in epidemio-
logic study as well as in patient care. These diag-
nostic aids do not change the philosophical
approach to measuring caries, although if reli-
able they will permit noncavitated lesions to be
detected at earlier stages of development.
Whether this is always necessary or not depends
on the aims of the given study and the purposes
for which the resulting data will be used.
ROOT CARIES
The criteria most frequently used to diagnose
root caries were first described in 1980.7 The
clinical examination was carried out after a
thorough prophylaxis, after which root caries
was diagnosed according to the criteria shown
in Box 15-3. Although these criteria have proved
to be versatile, there are several diagnostic issues
in root caries that have not yet been fully settled.
These problems include the lack of a universally
accepted case definition,8 difficulty in differen-
tiating active from nonactive lesions,27 and
uncertainties in diagnostic reliability.6
Root lesions are frequently difficult to detect
because many appear as small, discrete lesions
BOX 15-3 Criteria For Diagnosing Root Surface
Caries6
●
A discrete, well-defined, and discolored soft area is
present.
●
The explorer enters easily and displays some
resistance to withdrawal.
●
The lesion is located either at the cemento-enamel
junction or wholly on the root surface.
●
Restored root lesions are counted only if it was
obvious that the lesion originated at the cemento-
enamel junction or is confined to the root surface
completely.
on a single root surface rather than circumscrib-
ing a root.47 Although most lesions occur on
exposed root surfaces, around 15% of all root
lesions have been found on surfaces without
gingival recession, although of course there is
loss of periodontal attachment.13,33,47 It is not
yet clear whether these root lesions form in peri-
odontal pockets or whether an exposed root
surface later becomes covered by the over-
growth of inflamed gingiva. Problems in locat-
ing the cemento-enamel junction because of
obliteration by restorations or calculus can add
to the diagnostic difficulties.27
The extent of root caries can be expressed as a
simple prevalence figure, meaning the propor-
tion of a defined population with at least one
root lesion, and as the mean number of carious
or restored root lesions per person (i.e., a DFS
count). To provide the most complete profile of
root caries activity, however, these values should
be accompanied by the number of missing teeth
and by Root Caries Index (RCI) scores.
The RCI, first described in 1980,26 was inten-
ded to make the simple prevalence measures
more specific by including the concept of teeth at
risk (in contrast to the DMF index). A tooth was
considered to be at risk of root caries if enough
gingival recession had occurred to expose part of
the cemental surface to the oral environment.
The RCI is computed by scoring root lesions and
restorations and noting teeth with gingival reces-
sion, according to the following formula:
(Root surfaces: decayed + filled) × 100
(Root surfaces with loss of periodontal attachment:
decayed + filled + sound)

Table 15-1 Proposed case definitions of early childhood caries and severe early childhood caries15
Age in Months Early Childhood Caries*
<12 1 or more dmf surfaces
12-23 1 or more dmf surfaces
24-35 1 or more dmf surfaces
36-47 1 or more dmf surfaces
48-59 1 or more dmf surfaces
60-71 1 or more dmf surfaces
*Any carious lesion, whether noncavitated (d1) or cavitated (d2-d4), tooth missing due to caries (m), or filled surface (f). Primary teeth
only.
The index can be computed for an individual,
for particular tooth types, or for a population at
large. An RCI of 7% means that, of all teeth with
gingival recession, 7% were decayed or filled on
the root surfaces. As with any index scores,
results are most useful if a distribution measure
is also presented. The RCI does not take into
account the time at risk of an exposed root sur-
face; a root surface that has been exposed for
years is obviously at more risk than one just
recently exposed.
The original description of the RCI acknowl-
edged the chance of underestimation due to
exclusion of subgingival lesions,26 but at the time
these were considered unusual. As noted earlier,
however, some 15% or more of root lesions since
recorded are subgingival. Accordingly, it is now
recommended that the RCI be applied to both
supragingival and subgingival lesions but that the
scores for each type of lesion be recorded
separately.28
EARLY CHILDHOOD CARIES
Early childhood caries (ECC) is the name given to
extensive carious attack in infants and young
children that seems to be associated with regu-
lar exposure to sugar, often from fluid in a bot-
tle. Its dietary associations have resulted in a
plethora of names for the condition: baby bot-
tle tooth decay, nursing caries, labial caries, and
others.24 This proliferation of names, some of
which include the presumed etiology, has not
helped our understanding of the condition, and
for that reason the name early childhood caries is
recommended.
15 Measuring Dental Caries 199
Severe Early Childhood Caries*
1 or more smooth dmf surfaces
1 or more smooth dmf surfaces
1 or more smooth dmf surfaces
1 or more cavitated, filled, or missing (due to caries) smooth
surfaces in primary maxillary anterior teeth or dmfs ≥4
1 or more cavitated, filled, or missing (due to caries) smooth
surfaces in primary maxillary anterior teeth or dmfs ≥5
1 or more cavitated, filled, or missing (due to caries) smooth
surfaces in primary maxillary anterior teeth or dmfs ≥6
A practical case definition of ECC has been
slow to develop, and measurement cannot be
validly carried out without a case definition. In
an effort to bring some order out of chaos, a
1999 workshop set age-related criteria for ECC.
The workshop took the view that any caries in
children was ECC, and to define the severe cate-
gories (i.e., obvious caries in incisors and
molars) that most dental people think of, the
workshop introduced the term severe early child-
hood caries (S-ECC). The suggested criteria for
these conditions are shown in Table 15-1.
These guidelines are a step in the right direc-
tion. Although some confusion may arise from
application of the term ECC to any caries in chil-
dren up to 6 years of age, the view that caries in
young children is not normal is one to be
encouraged. The inclusion of the age relation-
ship also helps to clarify our view of the condi-
tion. These guidelines will probably be refined
over time, but for now they are clearly a step for-
ward in research on the subject, and their use is
to be recommended.
CARIES TREATMENT NEEDS
Assessment of the caries treatment needs of a
group, at first glance, appears to be nothing
more than the D segment of a mean DMF score
assessed from a survey. This approach, however,
has been shown not to work for the following
reasons:
●
Criteria used to diagnose caries in a survey
usually are not the same as those used by
practitioners in forming a patient’s treat-
ment plan.
200 The Methods of Oral Epidemiology
●
Patients’ own perceived needs, level of
interest in their dental conditions, and abil-
ity or willingness to pay all influence the
level of treatment carried out.
●
A practitioner has to judge whether a minor
lesion will develop into a major lesion over
time, and whether a lesion in a primary
tooth can safely remain untreated for the
life of the tooth. A survey scores a tooth by
how it appears at the time of the survey.
●
Treatment philosophies change with
expanding knowledge and technologic
developments; a treatment that is standard
today may not be so tomorrow.
Because surveys are usually conducted under
less than ideal conditions, relative to the dental
office, surveys would be expected to detect fewer
carious lesions than practitioners do.5 However,
that begs the question of which assessment is
“correct.” Field surveys can miss early lesions,
but practitioners can also overtreat. To add to
the uncertainty, treatment plans for the same
patients have been shown to vary drastically
from dentist to dentist.4,17,39,40
The difficulties in determining treatment
need through survey were illustrated in an
important series of reports from Scotland. They
began with a 1978 national dental survey in
Britain, in the course of which 720 dentate
adults in Scotland agreed to permit their dental
records to be followed over subsequent years.
After 3 years, records showed that, although 863
teeth in this group had been assessed as needing
restorative care in the survey, 3108 actually had
been restored. One might think that this finding
could be explained by lesions missed under the
poorer survey conditions, but if that explana-
tion is accepted then the next finding has no
logic: of the 863 teeth classified as needing
restorative treatment in the survey, only 271
(31%) were among the 3108 restored.39 This
shows that the care carried out, rather than
being an extension of the survey results, in fact
bore no relation to them. Findings were similar
for prosthetic treatment.16
Dental needs in the United States were as-
sessed by examiners in the first National Health
and Nutrition Examination Survey (NHANES I)
of 1971-74, and 65% of the population were
judged as being in need of care.48 A similar
assessment was made in the first national survey
of schoolchildren in 1979-80, in which 37% of
schoolchildren were judged to be in need of
restorative care.49 The validity of these figures is
debatable, and they have received little use. In
later national surveys treatment needs assess-
ments were not carried out.50,51
WHO includes a subjective treatment need
assessment by the examiner as part of its
Pathfinder survey method,55 although it has
not been determined how well these estimates
approximate treatment actually carried out.
WHO also has developed a broad-based
approach to determining needs in low-income
countries through what it calls a situation analy-
sis, an enhancement of Pathfinder survey data
with information on population trends, school
enrollment figures, per capita income, and
health care resources.56
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 16 Measuring Periodontal Diseases
MEASURING GINGIVITIS
MEASURING PERIODONTITIS
PERIODONTAL TREATMENT NEEDS
Although the DMF (decayed, missing, and filled
teeth) index for caries has remained stable over
a 50-year period, the philosophical basis for
measuring periodontal diseases has changed
several times over a shorter time span. In the
early days of modern periodontal research (i.e.,
the 1950s and 1960s), “periodontal disease”
was viewed as a single entity that began with
gingivitis and progressed to periodontitis and
tooth loss. This view is now obsolete (see
Chapter 21), so that indexes based on it are con-
sidered invalid. The separate clinical measures
now used for gingivitis and periodontitis were
first described some 40 years ago, and they
are still important. They will likely be joined
soon by some measures based on molecular
biology as knowledge in this area continues to
grow rapidly.
MEASURING GINGIVITIS
Gingivitis is inflammation of the gingivae with-
out involvement of the deeper supporting tis-
sues. The oldest reversible index is the P-M-A
(standing for Papillary-Marginal-Attached),
which dates from immediately after World War
II.41 As the inflammatory process became better
understood, it gave way to the Gingival Index
(GI) of Löe and Silness38 in the early 1960s,
anindex that is still used. The GI grades the gin-
giva on the mesial, distal, buccal, and lingual
surfaces of the teeth. Each area is scored on an
ordinal scale of 0-3 according to the criteria
shown in Box 16-1. The GI has been used to
score selected teeth in the mouth56 as well as all
PLAQUE AND CALCULUS
PARTIAL-MOUTH PERIODONTAL
MEASUREMENTS
erupted teeth.37 The GI, an index of gingivitis
that takes no account of deeper changes in
the periodontium, is sufficiently sensitive to
distinguish between groups with little and with
severe gingivitis, although it may not discrimi-
nate as well between groups in the middle
ranges.
Gingival bleeding after gentle probing has
become a standard measure of gingivitis in clin-
ical trials. Although visual assessments of
inflammation (color, swelling) are subjective,
the appearance of spots of blood after the probe
is gently run around the gingival margin is more
sensitive21 and more objective in those sites that
are difficult to view directly.22 Validity against
the GI has also been demonstrated.43 The major
area of subjectivity with use of a gingival bleed-
ing index is the “gentle probing,” which has
been shown to vary between 3 and 130 g for dif-
ferent examiners.49
A further refinement of the bleeding indexes
came with the Eastman Interdental Bleeding
Index,14 which may be more sensitive than
other measures of papillary bleeding.15
Gingival bleeding measures that do not carry
any particular name are collectively designated
by the acronym BOP (bleeding on probing).
The use of gingival bleeding indexes, as
opposed to visual determination of gingivitis, is
not recommended in public health programs
for three reasons:
1. This degree of sensitivity is rarely required
in surveys, surveillance, or screening; it
may be needed in cohort and case-control
studies.
203
204 The Methods of Oral Epidemiology
BOX 16-1 Scores and Criteria for the Gingival
Index.38
0: Normal gingiva
1: Mild inflammation—slight change in color, slight
edema; no bleeding on probing
2: Moderate inflammation—redness, edema, and
glazing; bleeding on probing
3: Severe inflammation—marked redness and edema;
ulceration; tendency to spontaneous bleeding
2. Such indexes have uncertain discrimina-
tory power in field conditions.39
3. Concerns about infection control make
the deliberate inducement of gingival
bleeding outside the clinic hard to justify.
The Modified Gingival Index (MGI) was
developed to eliminate the use of bleeding on
probing while still providing high visual sensi-
tivity for incipient gingivitis.36 Gingivitis is an
area in which the development of valid nonclin-
ical measures would be highly beneficial.
MEASURING PERIODONTITIS
Periodontitis is a family of related diseases that
differ in natural history, and response to ther-
apy but that are characterized by a common
underlying chain of events.48 These commonal-
ities, and their clinical expression, permit valid
clinical measurement by similar procedures,
basically measurement of clinical attachment
loss (CAL) and probing depth. Periodontitis is
a bacterially induced inflammation of the gin-
gival tissues together with some loss of both
the attachment of the periodontal ligament
and bony support. The clinical manifestations
of periodontitis come from the interaction
between bacterial infection and the host
response.
Many early epidemiologic studies of peri-
odontal diseases were based on radiographic
surveys of alveolar bone loss.16,54,55 However,
radiography, although a standard diagnostic
procedure in periodontitis clinical trials and
patient care, is impractical and probably unethi-
cal in field studies. The attempt was therefore
made to develop reversible indexes that were
both sensitive and clinically manageable in
field conditions. In this group, the most widely
used periodontal index for many years was the
Periodontal Index (PI), first described by
Russell in 1956.53
The PI was a composite index, meaning that
it scored both gingivitis and periodontitis on
the same scale. This represented the thinking of
the time, but modern understanding has
shown the PI to be invalid because it does not
include evaluation of CAL, grades all pockets of
3 mm or more equally, and scores gingivitis
and periodontitis on the same weighted scale.
Its compression of all information into a group
mean also fails to illuminate the disease distri-
bution, and a primary research interest today is
why some people have no disease and others
have severe disease. However, in the 1960s, the
PI was viewed as an ideal field index and was
used in a series of epidemiologic studies that
correlated disease scores with clinical and
social determinants. These correlations (see
Chapter 21) soon became accepted as basic
knowledge.
The same fundamental problem of a compos-
ite index was evident in the Periodontal Disease
Index (PDI), intended as a more sensitive ver-
sion of the PI for use in clinical trials.51 Although
the PDI is also no longer used, the indirect
method of measuring CAL that Ramfjord
described then is still employed today. The PDI
also gave us the “Ramfjord teeth,” a set of six
teeth taken to represent the whole mouth during
examination. The Ramfjord teeth are the maxil-
lary right first molar, left central incisor, and left
first bicuspid, and the mandibular left first
molar, right central incisor, and right first bicus-
pid. Ramfjord chose this group of teeth to save
time in clinical examinations. (Partial-mouth
recording is discussed later in this chapter.)
In field studies today periodontitis is still
measured by Ramfjord’s technique for the indi-
rect measurement of CAL.51 The approach is
shown graphically in Fig. 16-1. First, the exam-
iner measures probing depth from the gingival
crest to the base of the pocket. Second, the
cemento-enamel junction is located and the
depth from this junction to the gingival crest is
recorded. The difference between these values
gives an indirect measure of CAL. These meas-
urements are usually carried out at between two
and six sites per tooth, depending on the pur-
 16 Measuring Periodontal Diseases 205

A B B
A C
C = zero

1 2

A = Gingival crest to base of

pocket

B = Gingival crest to cemento-

enamel junction
B C = A minus B
C
A (Note: B is negative in example 3)

Fig. 16-1 Indirect method of measuring loss of periodontal attachment and pocket depth.51

pose of the study, either for selected teeth or for ●

the whole dentition. It is an exacting process:
measuring six sites per tooth for an intact denti-
tion can take 30-40 minutes per examination,
even for an experienced examiner.
The Extent and Severity Index (ESI) records
the percentage of sites with a CAL greater than
1 mm and the mean CAL for those affected
sites.13 When amended to set a cutoff value of
2 mm, it has yielded some useful summary
information.9 Despite its name, the ESI is a
method of summarizing data rather than a true
index. Its measurements are made by the
Ramfjord method.
Measurement of any disease is based on a
case definition, and the uncertainty in the case
definition for periodontitis is clearly part of the
reason we still use a recording procedure that is
almost 50 years old. A case definition for peri-
odontitis needs to establish the following:
●
What depth of CAL at any one site consti-
tutes evidence of disease processes
How many such sites need to be present in
a mouth to establish disease presence
●
How probing depth and BOP are to be
included in the case definition
In addressing the first issue, allowance also
must be make for examiner variation, which
can confuse efforts to measure CAL progression.
Even though measurements of pocket depth are
repeatable to within 1 mm more than 90% of
the time,29 the standard deviation of repeated
CAL measurements of the same site by an expe-
rienced examiner with a manual probe is
around 0.8 mm.24 Accordingly, change in
attachment level in a clinical study must be at
least 2 mm (i.e., two to three times the standard
deviation) before the investigators can be confi-
dent that they are seeing real change rather than
measurement error.25,34 CAL progression of at
least 3 mm over a given time period has been
the criterion for change in some studies.11,24,26
Even the introduction of computerized, con-
stant-force probes28 has not changed these
206 The Methods of Oral Epidemiology
issues much. Computerized probes are widely
used in clinical studies,52 but there is little dif-
ference in the reliability of measurements taken
with manual and with computerized probes for
most examiners.23,45
The problems inherent in clinical measure-
ment have led researchers to look for markers of
periodontitis. The most promising candidates
are the inflammatory cytokines expressed in
gingival crevicular fluid (GCF) as part of the
host response to inflammation, a number of
which have been associated with active dis-
ease.44,46 These cytokines include prostaglandin
E2, tumor necrosis factor-α, interleukin-1α,
interleukin-1β, and others. Although it has been
documented for some time that these and other
constituents of GCF are associated with inflam-
matory response,31-33 actually quantifying these
associations and determining the sensitivity of
the measures (i.e., the extent to which the quan-
tity of expressed cytokine increases or decreases
as inflammation increases or decreases) is prov-
ing difficult. To date, measurement of periodon-
titis by means of inflammatory cytokines in
GCF is still experimental, but this field is devel-
oping rapidly, and practical and efficient tests
are likely to emerge.
PERIODONTAL TREATMENT NEEDS
Any assessment of periodontal treatment needs
in a population has the same limitations that
are seen with caries. Treatment plans are subjec-
tive, often depending on some dentist-patient
factors that are not part of a clinical examina-
tion, and standard treatment for a given condi-
tion can change quickly as knowledge develops
(e.g., treatment of periodontal pockets has sub-
stantially shifted from surgical removal of pock-
ets to scaling and root planing). Even so, a
number of methods aimed at assessing peri-
odontal treatment needs have been developed
over the years,10,58 culminating in the
Community Periodontal Index of Treatment
Needs (CPITN).
The CPITN was first described in 1982,3 and
with some promotion by the World Health
Organization (WHO) it received worldwide
use.2 It differs from earlier indexes in several
ways. The most obvious is that it requires use of a
special periodontal probe, which has a 0.5 mm
diameter ball at its tip, a black band for visibility
between 3.5 mm and 5.5 mm, and circular
markings at 8.5 mm and 11.5 mm. The purpose
of the ball is to assist in feeling subgingival calcu-
lus and to help prevent the probe from being
pushed through inflammatory tissue at the base
of a pocket. Probing pressure is recommended to
be no more than 20 g (described as the pressure
at which the probe can be inserted under a fin-
gernail without discomfort). Another difference
is that the CPITN originally was used to catego-
rize people into treatment-need groups rather
than to compute mean values. Codes to be used
with the index are shown in Box 16-2.
Widespread use of the CPITN has produced
substantial contributions to WHO’s Global
Oral Health Data Bank (see Chapter 21), and a
number of national dental associations have
encouraged use of the CPITN by its practitioner
members. In the United States, the Indian
Health Service used the CPITN in its treatment
planning for some years. Then the American
Dental Association began to promote a slightly
modified version known as the Periodontal
Screening Record (PSR).42 Another modifica-
tion of the CPITN appeared in Britain, called
the British Periodontal Examination, or BPE.47
The validity of the CPITN/PSR continues to be
debated; it appears that the index underesti-
mates in some areas and overestimates in oth-
ers.5-7 The CPITN/PSR is not a research tool and
thus should not be used as a measure of peri-
odontitis in research studies.8
The index is now referred to as the
Community Periodontal Index, or CPI. This
BOX 16-2 Codes and Criteria for the Community
Periodontal Index Described by the World Health
Organization59
0: Healthy gingiva.
1: Bleeding observed, directly or by using the mouth
mirror, after “sensing” (i.e., gentle probing).
2: Calculus felt during probing but all the black area of
the probe visible (3.5-5.5 mm from ball tip).
3: Pocket 4 or 5 mm (gingival margin situated on
black area of probe, i.e., 3.5-5.5 mm from probe
tip).
4: Pocket >6 mm (black area of probe not visible).
X: Excluded segment (less than two teeth present).
9: Not recorded.

change followed a workshop on the index in
Manila in 1994.2,30,47 The workshop recom-
mended that the CPI remain the global stan-
dard for data on health planning but that the
treatment need codes be eliminated because
they had become obsolete in view of current
treatment methods.47 Hence the metamorpho-
sis of the CPITN into the CPI. The current ver-
sion of the CPI even includes optional use of
CAL measurements.59
PLAQUE AND CALCULUS
Plaque and calculus are still measured in terms
of quantity rather than quality, so most indexes
are variations on that theme. These indexes have
been around for some years.
The Simplified Oral Hygiene Index
(OHI-S)19,20 had wide use in surveys. It is quick
and practical to apply, although it lacks sensitiv-
ity. The OHI-S scores calculus and plaque
together, both supragingivally and subgingivally.
The current focus on subgingival, rather than
supragingival, plaque and calculus renders this
index obsolete for most purposes today. A spin-
off index is the Patient Hygiene Performance
(PHP), in which plaque deposits are recorded
in five different tooth surface zones after use of
a disclosing tablet.50
Silness and Löe56 developed the Plaque
Index (PlI) to be used along with their GI. The
same surfaces of the same teeth are scored as in
the GI and a 0-3 ordinal scale is again used. The
principal difference in approach between the
PlI and the OHI-S is that the PlI scores plaque
according to its thickness at the gingival margin
rather than its coronal extent, a measure
claimed to be more valid.4 The PlI is still used;
codes and criteria for this index are shown
in Box 16-3.
WHO, after several earlier efforts to develop a
simple measure of oral hygiene status,58 settled
for the measure of subgingival calculus that is
part of the CPI.59 Soft plaque deposits are
ignored in the CPI. Because calculus appears to
be the aspect of oral hygiene most closely asso-
ciated with periodontitis,40 a simple measure
of its presence or absence, such as WHO uses
in the CPI, is sufficient for many purposes.
As always, however, the index chosen depends
on the purpose of the given survey and the way
the data are to be used.
16 Measuring Periodontal Diseases 207
BOX 16-3 Scores and Criteria for the Plaque
Index37
0: No plaque in the gingival area.
1: A film of plaque adhering to the free gingival margin
and adjacent area of the tooth. The plaque may only
be recognized by running a probe across the tooth
surface.
2: Moderate accumulation of soft deposits within the
gingival pocket, on the gingival margin and/or
adjacent tooth surface, which can be seen by the
naked eye.
3: Abundance of soft matter within the gingival pocket
and/or on the gingival margin and adjacent tooth
surface.
The Volpe-Manhold Index, or VMI,57 has
been widely used in the United States in trials to
test agents for plaque control and calculus inhi-
bition.35 It is intended to score new deposits of
supragingival calculus, following a prophylaxis
to remove all calculus, in clinical trials. (The rea-
soning is that all new calculus over a 3-month
period, the approximate length of a clinical trial
to test calculus-inhibiting products, will be
supragingival.) The VMI scores calculus deposits
on three planes (lingual, distal, and mesial) of
each of the lower six anterior teeth. A probe
is used to measure the linear extent of calculus
in increments of 0.5 mm, from 0 to 5 mm.
The tooth score is the sum of the scores in the
three planes; patient total score is the sum of
the tooth scores.
PARTIAL-MOUTH PERIODONTAL
MEASUREMENTS
Because full-mouth examinations for gingival
bleeding, CAL, plaque, and calculus can be time
consuming, investigators have tried using vari-
ous indexes on a subset of teeth to save time.
The expectation is that the subset of teeth will
act as a representative sample of all teeth in the
mouth, yielding information that can be
applied to the whole mouth but taking much
less time to examine. Partial-mouth recording
was pioneered by Ramfjord with the Ramfjord
teeth subset in 1959,51 and the CPI uses it today.
There is agreement that partial-mouth record-
ing is valid for assessing plaque formation and
208 The Methods of Oral Epidemiology
gingivitis,1,17,18,27 both of which are generalized
conditions. Partial-mouth recording is less satis-
factory for the site-specific conditions of CAL
and pocketing, for which systematic underre-
porting occurs with this method.1,6,17,27 Partial-
mouth recording is adequate for surveys in
which a degree of underestimation is an accept-
able trade-off for lower costs, but it is not recom-
mended for use in clinical trials or in any other
situation that demands a high degree of preci-
sion in the data.
The National Institute of Dental and
Craniofacial Research was criticized for the
method it chose for measuring periodontitis in
the National Survey of Employed Adults and
Seniors in 1985-86. Two randomly chosen
quadrants were examined, one maxillary and
one mandibular, and probing depth and CAL
were measured at two sites, the mesiobuccal
and buccal. Critics thought this method would
underestimate the true prevalence of periodon-
titis for the following reasons:
●
The site specificity of periodontitis meant
that severity would be underestimated if
only two quadrants instead of the whole
mouth were measured.
●
Severity would be further underestimated
by measurement of only two sites per
tooth, and no lingual site at that.
That underestimation may be real, but the
same method was used for measuring peri-
odontitis in the third National Health and
Nutrition Examination Survey (NHANES III) of
1988-94.12 In fairness, the method may be suf-
ficiently valid for the purposes of the survey,
and it represents a great savings of time (and
hence cost). It is a pragmatic measure, not rec-
ommended for analytic research but adequate
for surveillance.
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 17 Measuring Dental Fluorosis
DEAN’S FLUOROSIS INDEX
TOOTH SURFACE INDEX OF FLUOROSIS
THYLSTRUP-FEJERSKOV INDEX
This chapter describes methods for measuring
dental fluorosis. Dental fluorosis is a hypomin-
eralization of the dental enamel caused by
excessive ingestion of fluoride during tooth
development.13 Depending on the quantity and
timing of fluoride ingestion during this period,
the clinical appearance of fluorosis can range
from barely noticeable changes to an ugly
brown stain with pitting and flaking of friable
enamel.
DEAN’S FLUOROSIS INDEX
An index of fluorosis was needed when the ini-
tial investigations of fluorosis began in the
1930s (see Chapter 22). Dean’s first Fluorosis
Index set criteria for categorizing dental fluoro-
sis on a seven-point ordinal scale: normal, ques-
tionable, very mild, mild, moderate, moderately
severe, and severe. Dean used this seven-point
scale for his Fluorosis Index for some years,3,8
but by 1939 his experience led him to combine
the “moderately severe” and “severe” categories
into a single “severe” category.9 By 1942 Dean
had revised his Fluorosis Index into a six-point
scale, including normal or unaffected enamel,4
that still finds some use today. Dean’s criteria
for his revised version of the Fluorosis Index are
shown in Box 17-1.
A spin-off of the Fluorosis Index was the
Community Fluorosis Index (CFI), which Dean
defined in 1935 by assigning arbitrary numeri-
cal values to his seven-point ordinal scale, again
ranging from no fluorosis and borderline to
severe and very severe.6 Fig. 17-1 shows the dis-
210
FLUOROSIS RISK INDEX
DEVELOPMENTAL DEFECTS OF DENTAL
ENAMEL INDEX
tributional data from 10 communities7 on which
he based the CFI. Dean related this index to the
concentration of fluoride in a water supply and
was able to show a linear correlation, as one of
his original charts demonstrates (Fig. 17-2).
Dean also stated, although only in a footnote,
that CFI scores below 0.4 were of “no public
health significance.”5 With cosmetic awareness
likely to be greater now than it was in the 1930s,
however, Dean’s personal assessment of the
public health significance of fluorosis may be
less relevant today.
TOOTH SURFACE INDEX
OF FLUOROSIS
Fluorosis was the subject of surprisingly little
study after the initial investigations of con-
trolled water fluoridation21 until the 1980s,
when research was spurred by suggestions that
its prevalence might be increasing.16 During the
1980s, the Tooth Surface Index of Fluorosis
(TSIF) was developed and used by researchers at
the National Institute of Dental Research.10,15
Criteria for the TSIF are shown in Box 17-2. The
TSIF scale is probably more sensitive than
Dean’s index in identifying the mildest forms of
fluorosis. The TSIF ascribes a score on a scale of
0-7 to each tooth surface in the mouth, whereas
Dean’s index applies only to the two most
affected teeth in the mouth. The World Health
Organization, however, still recommends use of
Dean’s Fluorosis Index in its basic survey man-
ual.26 TSIF results are given as an ordinal distri-
bution rather than as mean scores.
 17 Measuring Dental Fluorosis 211

Mean
Annual
Size Percentage Distribution of Sample
Fluoride
City of According to Severity of Affection
(F)
Sample
Content
(PPM) 0 10 20 30 40 50 60 70 80 90
Lubbock, TX 176 4.4
Amarillo, TX 168 3.9
Conway, SC 59 4.0
Plainview, TX 78 2.9
Colorado Springs, CO 79 2.5
Galesburg, IL 57 1.8
Monmouth, IL 38 1.7
Mullins, SC 47 0.9
Big Springs, TX 68 0.7
Pueblo, CO 83 0.6

Moderate to severe Mild Very mild Questionable Normal

Fig. 17-1 Data from Dean’s studies to show the distribution of fluorosis severity in relation to fluoride concentration
of the drinking water in 10 communities.8

BOX 17-1 Criteria for Dean’s Fluorosis Index4

Normal:
The enamel represents the usual translucent semivitriform type of structure. The surface is smooth, glossy, and
usually of a pale creamy white color.
Questionable:
The enamel discloses slight aberrations from the translucency of normal enamel, ranging from a few white flecks to
occasional white spots. This classification is utilized in those instances in which a definite diagnosis of the mildest
form of fluorosis is not warranted and a classification of “normal” not justified.
Very mild:
Small, opaque, paper-white areas scattered irregularly over the tooth but not involving as much as approximately 25%
of the tooth surface. Frequently included in this classification are teeth showing no more than about 1-2 mm of
white opacity at the tip of the summit of the cusps of the bicuspids or second molars.
Mild:
The white opaque areas in the enamel of the teeth are more extensive but do not involve as much as 50% of the tooth.
Moderate:
All enamel surfaces of the teeth are affected, and surfaces subject to attrition show marked wear. Brown stain is
frequently a disfiguring feature.
Severe:
Includes teeth formerly classified as “moderately severe” and “severe.” All enamel surfaces are affected and hypoplasia
is so marked that the general form of the tooth may be altered. The major diagnostic sign of this classification is the
discrete or confluent pitting. Brown stains are widespread and teeth often present a corroded appearance.

The TSIF is viewed as a public health index
rather than as a research tool. It does not call for
drying of the teeth prior to scoring, on the
grounds that when the appearance of teeth is
judged in everyday life it is done so with the
teeth wet. The very mildest forms of fluorosis
are therefore likely to be missed with the TSIF.
The previous discussions of fluorosis indexes
concern fluorosis in the permanent denti-
tion, because fluorosis was for a long time
thought not to occur at all in the primary teeth.
It does, however, and the TSIF has also
been used to record fluorosis in the primary
dentition.17,25
212 The Methods of Oral Epidemiology
of the communal water supply having
the indicated fluoride concentration
associated with the continued use
Index of dental fluorosis found 3
0
0 1
Fluoride (F) concentration of communal water supply in parts per million (PPM)
Fig. 17-2 Data from Dean’s studies to show the relation between mean Fluorosis Index scores and the fluoride con-
centration of the drinking water.4
BOX 17-2 Clinical Criteria and Categorizations for
the Tooth Surface Index of Fluorosis15
0: Enamel shows no evidence of fluorosis.
1: Enamel shows definite evidence of fluorosis,
namely, areas with parchment-white color that total
less than one third of the visible enamel surface.
This category includes fluorosis confined only to
incisal edges of anterior teeth and cusp tips of
posterior teeth (“snowcapping”).
2: Parchment-white fluorosis totals at least one third
of the visible surface, but less than two thirds.
3: Parchment-white fluorosis totals at least two thirds
of the visible surface.
4: Enamel shows staining in conjunction with any of
the preceding levels of fluorosis. Staining is defined
as an area of definite discoloration that may range
from light to very dark brown.
5: Discrete pitting of the enamel exists,
unaccompanied by evidence of staining of intact
enamel. A pit is defined as a definite physical defect
in the enamel surface with a rough floor that is
surrounded by a wall of intact enamel. The pitted
area is usually stained or differs in color from the
surrounding enamel.
6: Both discrete pitting and staining of the intact
enamel exist.
7: Confluent pitting of the enamel surface exists. Large
areas of enamel may be missing and the anatomy of
the tooth may be altered. Dark brown stain is
usually present.
2 3 4 5 6 7 8 14
THYLSTRUP-FEJERSKOV INDEX
With studies of fluorosis being carried out in
many regions of the world, Dean’s Fluorosis
Index inevitably became modified to meet spe-
cific needs; for example, its sensitivity at the
higher end of the scale was increased to han-
dle situations in which fluorosis was more
severe than any with which Dean had to deal.24
The resulting Thylstrup-Fejerskov (TF) index
has a stronger biologic basis than Dean’s more
or less arbitrary index, because the index scores
were developed by relating them to histologic
features of affected enamel. The criteria for the
TF index are shown in Box 17-3. Because its use
necessitates drying of the teeth, the TF index is
the most sensitive of existing indexes. At the
same time, it requires assessment of only one
surface per tooth because fluorosis affects all
tooth surfaces equally.14 It can be used on
selected teeth or the whole dentition, and
results again are expressed as distributions
rather than as mean scores. An example of a TF
distribution is shown in Fig. 17-3.
FLUOROSIS RISK INDEX
The Fluorosis Risk Index (FRI)19 is designed for
use in analytic studies that seek to identify risk
factors for fluorosis; it explicitly recognizes that
the risk of fluorosis is related to fluoride expo-
sure at particular stages of dentition develop-
ment. It divides the buccal and occlusal surfaces
 17 Measuring Dental Fluorosis 213

BOX 17-3 Clinical Criteria and Scoring for the Thylstrup-Fejerskov Fluorosis Index24

0: Normal translucency of enamel remains after prolonged air-drying.

1: Narrow white lines located corresponding to the perikymata.
2: Smooth surfaces:
More pronounced lines of opacity that follow the perikymata. Occasionally confluence of adjacent lines.
Occlusal surfaces:
Scattered areas of opacity <2 mm in diameter and pronounced opacity of cuspal ridges.
3: Smooth surfaces:
Merging and irregular cloudy areas of opacity. Accentuated drawing of perikymata often visible between
opacities.
Occlusal surfaces:
Confluent areas of marked opacity. Worn areas appear almost normal but usually circumscribed by a rim of
opaque enamel.
4: Smooth surfaces:
The entire surface exhibits marked opacity or appears chalky white. Parts of surface exposed to attrition appear
less affected.
Occlusal surfaces:
Entire surface exhibits marked opacity. Attrition is often pronounced shortly after eruption.
5: Smooth and occlusal surfaces:
Entire surface displays marked opacity with focal loss of outermost enamel (pits) <2 mm in diameter.
6: Smooth surfaces:
Pits are regularly arranged in horizontal bands <2 mm in vertical extension.
Occlusal surfaces:
Confluent areas <3 mm in diameter exhibit loss of enamel. Marked attrition.
7: Smooth surfaces:
Loss of outermost enamel in irregular areas involving <1⁄2 of entire surface.
Occlusal surfaces:
Changes in the morphology caused by merging pits and marked attrition.
8: Smooth and occlusal surfaces:
Loss of outermost enamel involving >1⁄2 of surface.
9: Smooth and occlusal surfaces:
Loss of main part of enamel with change in anatomic appearance of surface. Cervical rim of almost unaffected
enamel is often noted.

of each permanent tooth into four zones based
on the age at which calcification begins and
selectively classifies each zone into one of two
categories.18 There is also a tight case definition
of fluorosis. When related to the history of fluo-
ride exposure, fluorosis that develops during
the maturation phase of enamel can be differen-
tiated from that which develops earlier. Wider
use of this index is likely in studies on fluorosis
risk factors.
DEVELOPMENTAL DEFECTS
OF DENTAL ENAMEL INDEX
The intent of the Developmental Defects of
Dental Enamel (DDE) index was to avoid the
need to diagnose fluorosis before recording
enamel opacities, a requirement that some
think may introduce measurement bias.12 The
DDE index has been used a number of times
since its introduction,2,11,22,23 but the large
amount of data generated has led to problems
in presenting results in a meaningful fashion.
Following a national survey of children in
Ireland, modifications to the DDE index were
suggested to make it simpler.1
Russell20 addressed the same issue of distin-
guishing between milder forms of fluorosis and
nonfluoride enamel opacities, and provided a
description of differential diagnostic features as
shown in Table 17-1. An accurate history of
drinking water sources, as well as of the use of
214 The Methods of Oral Epidemiology

100

Less severe
80 More severe

60
Percent

40

20

0
0 1 2 3 4+

Fluorosis severity score

(TF index)
Fig. 17-3 Hypothetical data to show the distribution of fluorosis in two U.S. child populations, as measured by the
Thylstrup-Fejerskov (TF) index.

Table 17-1 Differential diagnosis between milder forms of dental fluorosis (questionable, very mild, and mild)
and nonfluoride opacities of enamel20
Characteristic of
Enamel Opacities Milder Forms of Fluorosis Nonfluoride Opacities

Area affected Usually seen on or near tips of cusps
or incisal edges.
Shape of lesion Resembles line shading in pencil sketch;
lines follow incremental lines in enamel, form
irregular caps on cusps.
Demarcation Shades off imperceptibly into surrounding
normal enamel.
Color Slightly more opaque than normal enamel;
paper white. Incisal edges, tips of cusps
may have frosted appearance. Does not show
stain at time of eruption (in these milder
degrees, rarely at any time).
Teeth affected Most frequent on teeth that calcify slowly
(cuspids, bicuspids, second and third molars).
Rare on lower incisors. Usually seen on six or
eight homologous teeth. Extremely rare in
deciduous teeth.
Gross hypoplasia None. Pitting of enamel does not occur in the
milder forms. Enamel surface has glazed
appearance, is smooth to point of explorer.
Detection Often invisible under strong light; most easily
detected by line of sight tangential to tooth
crown.
Usually centered in smooth surface;
may affect entire crown.
Often round or oval.
Clearly differentiated from adjacent
normal enamel.
Usually pigmented at time of eruption;
often creamy yellow to dark reddish
orange.
Any tooth may be affected. Frequent
on labial surfaces of lower incisors.
May occur singly. Usually one to
three teeth affected. Common in
deciduous teeth.
Absent to severe. Enamel surface may
seem etched, be rough to explorer.
Seen most easily under strong light on
line of sight perpendicular to tooth
surface.

fluoride tablets, toothpaste, and rinses, should
be sought by practitioners as an aid to diagnos-
ing the nature of enamel disturbances in
patients.
REFERENCES
1. Clarkson J, O’Mullane D. A modified DDE index for
use in epidemiological studies of enamel defects. J Dent
Res 1989;68:445-50.
2. Cutress TW, Suckling GW, Pearce EIF, Ball BE. Defects
of tooth enamel in children in fluoridated and non-
fluoridated water areas of Auckland. N Z Dent J
1985;81:12-9.
3. Dean HT. Chronic endemic dental fluorosis (mottled
enamel). In: Gordon SM, ed: Dental science and dental
art. Philadelphia: Lea and Febiger, 1938:387-414.
4. Dean HT. The investigation of physiological effects by
the epidemiological method. In: Moulton FR, ed:
Fluorine and dental health. Washington DC: American
Association for the Advancement of Science, 1942:
23-71.
5. Dean HT. Epidemiological studies in the United States.
In: Moulton FR, ed: Dental caries and fluorine.
Washington DC: American Association for the
Advancement of Science, 1946:5-31.
6. Dean HT, Dixon RM, Cohen C. Mottled enamel in
Texas. Public Health Rep 1935;50:424-42.
7. Dean HT, Elvove E. Some epidemiological aspects of
chronic endemic dental fluorosis. Am J Public Health
1936;26:567-75.
8. Dean HT, Elvove E. Further studies on the minimal
threshold of chronic endemic dental fluorosis. Public
Health Rep 1937;52:1249-64.
9. Dean HT, Elvove E, Poston RF. Mottled enamel in South
Dakota. Public Health Rep 1939;54:212-28.
10. Driscoll WS, Horowitz HS, Meyers RJ, et al. Prevalence
of dental caries and dental fluorosis in areas with negli-
gible, optimal, and above-optimal fluoride concentra-
tions in drinking water. J Am Dent Assoc
1986;113:29-33.
11. Dummer PM, Kingdon A, Kingdon R. Prevalence
of enamel developmental defects in a group of 11- and
12-year-old children in South Wales. Community Dent
Oral Epidemiol 1986;14:119-22.
12. Fédération Dentaire Internationale, Commission on
Oral Research and Epidemiology. An epidemiological
17 Measuring Dental Fluorosis 215
index of developmental defects of dental enamel (DDE
index). Int Dent J 1982;32:159-67.
13. Fejerskov O, Manji F, Baelum V. The nature and mecha-
nisms of dental fluorosis in man. J Dent Res
1990;69(Spec Issue):692-700.
14. Fejerskov O, Manji F, Baelum V, Møller IJ. Dental fluo-
rosis: A handbook for health workers. Copenhagen:
Munksgaard, 1988.
15. Horowitz HS, Driscoll WS, Meyers RJ, et al. A new
method for assessing the prevalence of dental fluoro-
sis—the Tooth Surface Index of Fluorosis. J Am Dent
Assoc 1984;109:37-41.
16. Leverett DH. Fluorides and the changing prevalence of
dental caries. Science 1982;217:26-30.
17. Levy SM, Hillis SL, Warren JJ, et al. Primary tooth fluo-
rosis and fluoride intake during the first year of life.
Community Dent Oral Epidemiol 2002;30:286-95.
18. Pendrys DG. The Fluorosis Risk Index: A method for
investigating risk factors. J Public Health Dent
1990;50:291-8.
19. Pendrys DG, Katz RV. Risk of enamel fluorosis associ-
ated with fluoride supplementation, infant formula,
and fluoride dentifrice use. Am J Epidemiol
1989;130:1199-1208.
20. Russell AL. The differential diagnosis of fluoride and
nonfluoride enamel opacities. Public Health Dent
1961;21:143-6.
21. Russell AL. Dental fluorosis in Grand Rapids during the
seventeenth year of fluoridation. J Am Dent Assoc
1962;65:608-12.
22. Suckling GW, Brown RH, Herbison GP. The prevalence
of defects of enamel in nine-year-old children in New
Zealand in a health and development study.
Community Dent Health 1985;2:303-13.
23. Suckling GW, Pearce EIF. Developmental defects of
enamel in a group of New Zealand children.
Community Dent Oral Epidemiol 1984;12:177-84.
24. Thylstrup A, Fejerskov O. Clinical appearance of dental
fluorosis in permanent teeth in relation to histologic
changes. Community Dent Oral Epidemiol
1978;6:315-28.
25. Warren JJ, Levy SM, Kanellis MJ. Prevalence of dental
fluorosis in the primary dentition. J Public Health Dent
2001;61:87-91.
26. World Health Organization. Oral health surveys; basic
methods. 4th ed. Geneva: WHO, 1997.
 18 Measuring Other Conditions
in Oral Epidemiology
MALOCCLUSION
ORAL CANCERS
Other conditions have been studied in oral epi-
demiology with varying amounts of success.
Some, like temporomandibular disorders, pres-
ent so many inherent difficulties that they will
probably always be extremely difficult to meas-
ure. Others such as soft tissue lesions other than
oral cancer and precancers (e.g., oral pemphi-
gus, lichen planus) have simply not attracted
much attention.
MALOCCLUSION
Malocclusion is a difficult entity to define because
individuals and cultures vary widely in percep-
tions of what constitutes a malocclusion prob-
lem. Quite a number of malocclusion indexes
have been devised, but probably because of this
perceptual problem, none has ever emerged as a
standard. These issues have not changed over the
years, and there are thoughtful, still valid com-
mentaries from the 1970s on the problems of
classifying and scoring malocclusions.13,15
Angle’s classification, which dates from the
nineteenth century,1 may still be useful in treat-
ment planning but is of no use in epidemiology
because it is a nominal categorization. Most
other indexes suffer from the limitation that
they record specific conditions (e.g., overbite,
posterior crossbite) rather than the status of the
whole occlusion. The Malalignment Index31
assesses rotation and tooth displacement,
whereas the Occlusal Feature Index24 records
crowding, cuspal interdigitation, and vertical
and horizontal overbite. The Handicapping
Labio-Lingual Deviations (HLD, which, interest-
ingly enough, is also the developer’s initials)
216
CLEFT LIP AND PALATE
ORAL HEALTH AND QUALITY OF LIFE
Index11 received considerable public health use
when it was applied to assess treatment needs
for a public orthodontic program in New York
State. Grainger developed the Treatment Priority
Index (TPI) for assessing treatment needs, an
index that was used once, but only once, in
a national study of orthodontic needs of chil-
dren.30 None of these indexes has seen much
use in the years beyond its introduction. One
modestly successful measure is the Occlusal
Index, or OI,29 which measures nine characteris-
tics: dental age, molar relation, overbite, overjet,
posterior crossbite, posterior open bite, tooth
displacement, midline relations, and missing
permanent maxillary incisors. Its use demands a
fair degree of examiner skill and training, but it
is probably closer to a complete malocclusion
index than those listed earlier.
In Europe the Index of Orthodontic
Treatment Need (IOTN) has received some use
since it was first introduced in 1989.4 It was
modified from an existing Swedish scale and
combines both a functional and an esthetic
measure. Functional occlusion is categorized
into five different grades, whereas the esthetic
measure uses a 10-point ordinal scale that
allows the individual to determine his own
esthetic perception of the dentition. The IOTN
has shown some promise for use in public
health19 but has not been widely adopted. The
Peer Assessment Rating (PAR) index is designed
to capture all the occlusal anomalies that might
be found in malocclusion in a single score.25
This sounds ambitious, but the PAR index has
been found to equal the OI in reliability.5 The
search still continues for an omnibus measure,
 18
and the Index of Complexity, Outcome, and
Need (ICON) arrived with the new millen-
nium.10 It has been shown to correlate well with
patients’ perceptions of esthetics, speech, func-
tion, and need for treatment.17
The very proliferation of these indexes
underlines the difficulties in measuring this
complex issue. The Fédération Dentaire
Internationale jumped on the bandwagon with
its attempt to develop an internationally
accepted index and simplified method of deter-
mining malocclusion.12 It was not successful;
the result was a carefully qualified method of
measuring occlusal traits. The index has been
used9 but seems to offer no more value than the
other indexes described.
The complexities of malocclusion, and the
frustrations that have grown up with the inade-
quacies of these indexes, have led many
researchers to believe that functional maloc-
clusion is virtually unmeasurable for epidemi-
ologic purposes. In terms of trying to interpret
group data on overbites, crowding, and other
clinical conditions, that may well be true.
Orthodontic indexes developed in the late
1980s, however, take a different philosophical
approach in that they assess esthetic rather
than clinical aspects of function. One is the
Dental Aesthetic Index (DAI), published in
1986 after years of testing.8 The DAI starts
from the premise that the impact of malocclu-
sion on other oral pathology is doubtful and
that the main benefit of orthodontic treatment
is its effect on the individual’s social and psy-
chological well-being. The DAI makes objec-
tive measurements of aesthetic acceptability
according to social norms, and it has been vali-
dated for this use in a number of different
countries. As noted earlier, the IOTN also
includes an esthetic component measured on a
10-point ordinal scale.
The World Health Organization, in its
Pathfinder survey protocol,32 suggests using
DAI criteria to record malocclusion in the fol-
lowing categories:
●
Missing incisor, canine, and bicuspid teeth
●
Incisal crowding in the maxillary and
mandibular anterior segments
●
Spacing in the maxillary and mandibular
anterior segments
●
Diastema between the two maxillary cen-
tral incisors
Measuring Other Conditions in Oral Epidemiology 217
●
Largest irregularity in the front four maxil-
lary anterior incisors (rotations or displace-
ment from normal alignment)
●
Largest irregularity in the front four
mandibular anterior incisors
●
Anterior maxillary and mandibular overjet
●
Vertical anterior open bite
●
Anteroposterior molar relation
ORAL CANCER
As with other cancers, occurrence of oral cancer
is usually expressed as a proportion or rate. The
age-adjusted rate of years of life lost from oral
cancer, for example, dropped from 23.1 per
100,000 population in 1970 to 19.9 per 100,000
in 1985.21 Five-year survival rates are also useful
cancer measures: a 5-year survival rate of 67%,
for example, means that 67% of persons in
whom the condition was diagnosed 5 years ear-
lier are still alive.
Cancer data are maintained in registries in
most (but not all) states; information is
reported to the registry by physicians and hospi-
tals. Some 11 of these population-based reg-
istries in the United States participate in the
Surveillance, Epidemiology, and End Results
(SEER) program, which is conducted by the
National Cancer Institute (see Chapter 4). The
SEER program is the nation’s principal source of
national estimates of site-specific cancer inci-
dence and trends, and is the primary source of
the research data used in epidemiologic studies.
CLEFT LIP AND PALATE
The occurrence of cleft lip and palate is also usu-
ally expressed as a proportion; about 1 infant in
700 births exhibits this condition.14 Soft tissue
abnormalities of various kinds, as well as the
more rare types of oral pathoses, are also most
suitably expressed as proportions or rates. Cleft
lip and palate, as a congenital abnormality, is
supposed to be recorded on birth certificates in
the United States, although such recording is
unfortunately far from universal.
ORAL HEALTH AND QUALITY OF LIFE
Although philosophically it is desirable to
measure health rather than disease, in practice
epidemiology concerns itself with measuring
218 The Methods of Oral Epidemiology
disease because health is so difficult to define in
operational terms (see Chapter 4). When a con-
cept is difficult to define, it is also difficult
to measure. Several extensive research efforts
have been made to develop an index of oral
health.6,7,16,20,22,23 These approaches have been
largely empiric, meaning that they have
been based on what dentists consider oral
health to be, and they require some form of
weighting of conditions to reflect their relative
seriousness. They do not take any subjective
measures into account.
Given that health is more than the absence of
disease, several commentators have argued that
an individual’s subjective assessment of his or
her own oral health is at least as valid as a den-
tist’s, and probably more so. This is a different
philosophical approach to disease measure-
ment, because subjective indicators and clinical
indicators of oral health are poorly correlated.18
The Oral Health Impact Profile (OHIP)
measures the social impact of oral conditions as
perceived by the individual and was derived ini-
tially from statements given by dental patients
in interviews. It was later refined and tested
extensively for validity and reliability.28 The
OHIP was originally developed as a 49-item
scale but later was shortened to a 14-item scale,
which measured oral health quality of life as
validly as the initial version26 and was easier to
work with.
Another index that has received widespread
use is the General Oral Health Assessment
Index (GOHAI), originally the Geriatric Oral
Health Assessment Index. The GOHAI is a 12-
item scale that assesses physical functions, psy-
chosocial functions, and pain or discomfort.2,3
Indexes like these have considerable potential
for ranking oral disorders in terms of their
impacts on peoples’ daily lives, thus broadening
our perspectives of oral health and aiding both
clinical treatment planning and research.
Objective measurement of caries or periodon-
titis appears relatively simple compared to assess-
ing the subjective impacts of oral disease and
disabilities on peoples’ lives. A 1996 conference
at Chapel Hill, North Carolina, explored the vari-
ous measures currently existing for assessing
quality of life.27 This conference was exploratory
and came to no general conclusions. It is likely to
be a baseline against which further developments
in this complex area are measured.
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Cosmos 1899;41:248-64.
2. Atchison KA. The General Oral Health Assessment
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North Carolina, Department of Dental Ecology, 1997.
3. Atchison KA, Dolan TA. Development of the geriatric
oral health assessment index. J Dent Educ
1990;54:680-7.
4. Brook PH, Shaw WC. The development of an index of
orthodontic treatment priority. Eur J Orthod
1989;11:309-20.
5. Buchanan IB, Shaw WC, Richmond S, et al. A compari-
son of the reliability and validity of the PAR Index and
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6. Bulman JS, Richards ND, Slack GL, Willcocks AJ.
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7. Burke FJ, Wilson NH. Measuring oral health: An histor-
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8. Cons NC, Jenny J, Kohaut FJ. DAI: The Dental Aesthetic
Index. Iowa City IA: University of Iowa, 1986.
9. Cons NC, Mruthyunjaya YC, Pollard ST. Distribution
of occlusal traits in a sample of 1,337 children, ages
15-18, residing in upstate New York. Int Dent J 1978;
28:154-64.
10. Daniels C, Richmond S. The development of the index
of complexity, outcome, and need (ICON). J Orthod
2000;27:149-62.
11. Draker HL. Handicapping labio-lingual deviations pro-
posed for public health purposes. Am J Orthod
1960;46:295-305.
12. Fédération Dentaire Internationale. Commission on
Classification and Statistics for Oral Conditions. A
method for measuring occlusal traits. Int Dent J
1973;23:530-7.
13. Foster TD. The public health interest in assessment for
orthodontic treatment. J Public Health Dent
1979;39:137-42.
14. Greene JC. Epidemiology of congenital clefts of the lip
and palate. Public Health Rep 1963;78:589-602.
15. Jago JD. The epidemiology of dental occlusion; a criti-
cal appraisal. J Public Health Dent 1974;34:80-93.
16. Koch AL, Gershen JA, Marcus M. A children’s oral
health status index based on dentists’ judgment. J Am
Dent Assoc 1985;110:36-42.
17. Koochek AR, Yeh MS, Rolfe B, Richmond S. The rela-
tionship between Index of Complexity, Outcome and
Need, and patients’ perceptions of malocclusion:
A study in general dental practice. Br Dent J 2001;
191:325-9.
18. Locker D, Slade GD. Association between clinical and
subjective indicators of oral health status in an older
adult population. Gerodontology 1994;11:108-14.
19. Lunn H, Richmond S, Mitropoulos C. The use of
the Index of Orthodontic Treatment Need (IOTN) as a
public health tool: A pilot study. Community Dent
Health 1993;10:111-21.
20. Marcus M, Koch AL, Gershen JA. Construction of a pop-
ulation index of adult oral health status derived from
 18
dentists’ preferences. J Public Health Dent 1983;43:
284-94.
21. Myers MH, Glockler Ries LA. Cancer patient survival
rates: SEER program results for 10 years of follow-up.
CA Cancer J Clin 1989;39:21-32.
22. Nikias MK, Sollecito WA, Fink R. An empirical
approach to developing multidimensional oral status
profiles. J Public Health Dent 1978;38:148-58.
23. Nikias MK, Sollecito WA, Fink R. An oral health index
based on ranking of oral status profiles by panels of den-
tal professionals. J Public Health Dent 1979;39: 16-26.
24. Poulton DR, Aaronson SA. The relationship between
occlusion and periodontal status. Am J Orthod 1961;
47:690-9.
25. Richmond S, Shaw WC, O’Brien KD, et al. The develop-
ment of the PAR Index (Peer Assessment Rating):
Reliability and validity. Eur J Orthod 1992;14:125-39.
26. Slade GD. Derivation and validation of a short-form
oral health impact profile. Community Dent Oral
Epidemiol 1997;25:284-90.
Measuring Other Conditions in Oral Epidemiology 219
27. Slade GD, ed. Measuring oral health and quality of life.
Chapel Hill NC: University of North Carolina, 1997.
28. Slade GD, Spencer AJ. Development and evaluation of
the Oral Health Impact Profile. Community Dent
Health 1994;11:3-11.
29. Summers CJ. The Occlusal Index; a system for identify-
ing and scoring occlusal disorders. Am J Orthod
1971;59:552-67.
30. US Public Health Service, National Center for Health
Statistics. Orthodontic treatment priority index. PHS
Publication No. 1000, Series 2 No. 25. Washington DC:
Government Printing Office, 1967.
31. Van Kirk LE Jr, Pennell EH. Assessment of malocclusion
in population groups. Am J Orthod 1959;45:752-8.
32. World Health Organization. Oral health surveys; basic
methods. 4th ed. Geneva: WHO, 1997.
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 19 Tooth Loss
HISTORICAL PICTURE
EDENTULISM
PARTIAL TOOTH LOSS
Tooth loss, especially total tooth loss or eden-
tulism, is the dental equivalent of death. Tooth
loss diminishes the quality of life, often sub-
stantially, and tooth loss is also related to
poorer general health.44 If retaining teeth were
just a matter of preventing disease conditions
then the issue would be reasonably straightfor-
ward, but it is more complicated than that.
Although loss of teeth is an end product of oral
disease, it is also a reflection of patient and den-
tist attitudes, the dentist-patient relationship,
the availability and accessibility of care, and the
prevailing philosophies of care. This chapter
reviews the issues and trends in tooth loss, and
the reasons why people lose teeth.
THE HISTORICAL PICTURE
For centuries, tooth loss was considered an
inevitable part of the human condition and was
thus generally accepted with resignation. Long
before dentistry emerged as a true profession
(see Chapter 1) the tooth-puller was a necessary
part of most cultures, sometimes based in a vil-
lage and sometimes plying an itinerant trade. As
the profession of dentistry evolved during the
nineteenth century, much of the work of dentists
was still devoted to tooth extraction. Caries was
rampant at this time (see Chapter 20), restora-
tive techniques crude and painful, prevention
unknown. As a result, people expected to lose
teeth and dentists expected to extract them.
Appalling oral health status marked by
extensive loss of teeth extended well into the
twentieth century in high-income countries.
REASONS FOR TOOTH LOSS
DENTAL CARE AND TOOTH LOSS
The oral condition of the millions drafted into
the armies of many countries during World War
I (1914-18) was generally dreadful. The re-
sponse of authorities was to extract more teeth,
so that troops preparing to bayonet each other
would not be bothered by toothache. Right after
the war, surveys in New York found that school-
girls ages 13-17 years had lost 13.5% of first
molars and 2.5% of second molars, whereas
adults of different ages had lost 22%-47% of
first molars.31,32 Things improved only slowly.
In the Hagerstown studies of 1938, 15-year-old
children averaged 1.1 lost permanent teeth per
child, 94% of which were first molars.37 Age-
specific tooth loss among white-collar working
adults in a large insurance office showed only
mild improvement between 1927 and 1942,20
and extensive tooth loss was still common
among World War II (1939-45) draftees in the
United States.49,53
By the beginning of the twenty-first century
tooth retention was much improved in all the
high-income nations. Change came about with
improvements in restorative dentistry (espe-
cially the development of the air-turbine dental
engine in the late 1950s), increasing affluence
and its accompanying positive attitudes toward
tooth retention, and significant research adv-
ances in preventing oral diseases. In that latter
context, the advent of water fluoridation (see
Chapter 25) was probably the most profound
influence, because it demonstrated to individu-
als and their families, in a way that dental treat-
ment could not, that dental caries and
subsequent tooth loss were not inevitable.
223
224 The Distribution of Oral Diseases and Conditions

EDENTULISM Table 19-1 Percentage of persons ages 65 and older

who are edentulous in 10 countries classified by
The sight of grandfather’s false teeth in a glass of water was a
national income status68
familiar one to several generations of Americans; the acquisi-
tion of false teeth was thought to go along with rheumatics, Percent National Income
constipation, sensory diminution, and loss of memory as a Country Edentulous Category*
normal part of growing old.13
Canada 58 High
That editorial comment from the mid-1980s Finland 41 High
Slovenia 16 High
conjured up an image that is fast becoming
United Kingdom 46 High
unknown to the present generation, because United States 24 High
edentulism continues to decline steadily in the Malaysia 57 Upper middle
United States12 and in other economically Albania 69 Lower middle
developed nations.36,50,54 Table 19-1 shows the Egypt 7 Lower middle
proportion of persons ages 65 and over who are Thailand 16 Lower middle
edentulous in 10 countries, along with the Indonesia 24 Low
national income category for each country. *As defined by the World Bank in World Bank Group, Data and sta-
Fig. 19-1 shows the proportion of adults, by age, tistics, Country groups, website: http://www.worldbank.
who are edentulous, as measured in national org/data/countryclass/classgroups.htm. Accessed December 19,
surveys in the United States in 1957-58, 1971, 2003.
1985-86, and 1988-94. These data indicate that
edentulism has declined consistently in each
age-group with each succeeding survey. The rel- The third National Health and Nutrition
ative decline in edentulism has been sharpest in Examination Survey (NHANES III) was con-
the younger age-groups, which suggests that ducted between 1988 and 1994, and collected
edentulism will become even rarer as today’s data from a representative sample of the popu-
younger cohorts grow older. lation of the United States. In NHANES III,

80
1957-58 1985-86
70 1971 1988-94

60

50
Percent

40

30

20

10

0
25-34 35-44 45-54 55-64 65-74 75+

Age-group

Fig. 19-1 Proportion of the U.S. population edentulous in 1957-58, 1971, 1985-86, and 1988-94 by age.58,59,61,63

10.5% of Americans ages 18 or older were
found to be edentulous.19 There were sharply
defined age-cohort differences: only some 1%
of 25- to 34-year-olds were edentulous com-
pared to 44% of those ages 75 years or older.43
One estimate of the decline in edentulism sug-
gested that by the year 2024 only 10% of
Americans ages 65-74 would be edentulous,67
compared to 28% edentulous in that age-group
in 1988-91.43 Those who will be in the 65-74
age-cohort in 2024 were in the 25- to 34-year-
old group from 1988 to 1991, a cohort benefit-
ing from the postfluoride age of prevention (see
Chapter 20). This steady decline in edentulism
among United States adults is expected to con-
tinue in spite of the aging of the population (see
Chapter 2).
Many people are puzzled by the apparently
slow rate of progress in decreasing edentulism
when we constantly hear of rapid improve-
ments in oral health status. The reason lies in
the nature of the condition. When the data in
Fig. 19-1 are considered, it can be noted that the
youngest individuals in the 75-and-older
cohort for 1988-94 were born in 1919, and
most were born earlier. The early adult years for
this group were during the Great Depression of
the 1930s, and many of them then served in
World War II. Indeed, it is probable that a good
proportion of this cohort first became edentu-
lous during that war, and they have been influ-
encing the statistics ever since. In time, these
aging cohorts will be replaced by the baby
boomers, who grew up in a totally different
world of affluence and modern disease preven-
tion, and with fundamentally more positive
attitudes toward tooth retention. Already the
emerging elderly cohorts (i.e., the 55-64 and
65-74 cohorts from the two most recent surveys
in Fig. 19-1) represent the new elderly, a term
coined to describe the post-World War II group
who have experienced material affluence,
higher education than their predecessors, and
more of the benefits of modern preventive
health care.24 The level of total tooth loss
among these age-groups in 1985-86 and 1988-
94 was already sharply lower than that in the
75-and-over groups in Fig. 19-1.
The importance of nondisease factors in
edentulism emerges from Table 19-1, which
shows that the proportion of edentulous indi-
viduals among the elderly bears little relation-
19 Tooth Loss 225
ship to national income, and from Table 19-2,
which shows the extent of total tooth loss
among adults ages 35-44 in nine high-income
countries in the 1968-77 period. The data in
Table 19-2, most of them coming from the first
International Collaborative Survey (ICS I) of
the mid-1970s,4 show a range in the proportion
of edentulous persons from one country to
another that is too high to be explained solely
in terms of dental disease; health beliefs and
societal attitudes must be operating here. At the
time the data in Table 19-2 were collected, there
was still quite a high proportion of adults in
New Zealand, for example, who attached no
stigma to wearing full dentures.18 In developing
countries, where access to Western-type dental
care is limited, edentulism is uncommon.5,22,41
We introduced the National Oral Health
Surveillance System in Chapter 4 and noted that
total tooth loss was one of the eight indicators
of oral health. The information is collected by
interview as part of the Behavioral Risk Factor
Surveillance System (see Chapter 4), and some
of the differences between states in proportion
of older people who are edentulous give us food
for thought. Data for a selection of 10 states,
chosen more or less arbitrarily to highlight the
interstate contrasts, are shown in Table 19-3.
Historically, there has been a higher degree
of edentulism among women than among men,
and women have tended to become edentulous
at a younger age.18,26,57,61 These historical gen-
der differences are not easy to explain; many
think they reflected dentist-patient relation-
ships more than disease occurrence. Data from
the 1980s and later, however, suggest that these
gender differences are fading, because there was
Table 19-2 Percentage of persons ages 35-44 who
were edentulous in nine countries, 1968-777,8,26,57
Community/Country Percent Edentulous
Yamanashi, Japan 0.0
Hannover, Germany 1.6
Trøndelag, Norway 6.4
Ontario, Canada 8.7
Baltimore, USA 10.6
Sydney, Australia 13.2
England and Wales 22.0
Scotland 35.0
Canterbury, New Zealand 35.7
226 The Distribution of Oral Diseases and Conditions
Table 19-3 Percentage of persons in 10 of the United
States, ages 65 and older, who are edentulous60
State Percent Edentulous
United States 24.4
Hawaii 15.9
Nevada 16.5
California 18.5
Michigan 21.8
Georgia 28.9
Arkansas 29.2
Maine 35.0
Indiana 36.2
West Virginia 43.2
Kentucky 44.3
no pattern of difference between men and
women in the various age-groups among the
4.2% of employed U.S. adults who were edentu-
lous in 1985-86.64 In the more representative
sample seen in NHANES III, there again was vir-
tually no difference between men and women
in the proportion edentulous.43
In the United States, there has historically
been a greater degree of edentulism among
whites than among African-Americans,61 per-
haps because whites have traditionally had bet-
ter access to dental care (see Chapter 2) and
thus were at greater risk of having teeth
extracted (see Dental Care and Tooth Loss later
this chapter). Like gender differences, however,
differences between the races have become less
distinct since the 1980s, perhaps because eden-
tulism overall is becoming so uncommon
among younger cohorts. In both the national
survey of 1985-86 and that of 1988-94, only a
slightly higher proportion of whites than
African-Americans were edentulous.43,64
Fig. 19-2 shows the proportions of edentulous
people by age in the various racial and ethnic
groups in the 1988-94 national survey. It can be
seen that only Mexican-Americans had notably
less edentulism than the other groups.
Edentulism is tightly related to socioeco-
nomic status (SES). These SES-related differ-
ences are found consistently in many societies
and probably reflect expectations and health
attitudes at least as much as occurrence of oral
diseases.23,25 Unpublished data from the 1985-
86 U.S. survey show that the strongest risk indi-
cator for edentulism in employed adults (other
than age) was SES: 10.2% of those with fewer
than 8 years of education were edentulous com-
pared to 1.6% of those with 13 or more years.
Fig. 19-3 shows the proportions of edentulous
persons in three income-level groupings, and
clear and predictable differences are seen
among them. Similar SES-related differences
have been demonstrated in regional studies in
the United States14,29 and in Europe.34
Edentulous people have also been found to
have more risk factors for cardiovascular disease
than dentate people,33 and it should not be sur-
prising that older people in good health enjoy
greater tooth retention than do people of the
same age in poor health.40,45
PARTIAL TOOTH LOSS
Like edentulism, the extent of partial tooth loss
has been diminishing in the United States as
caries comes under control, more and better
treatment becomes available, and attitudes
toward tooth retention improve with increasing
affluence. In contrast to edentulism, in which
attitudes are a major factor in a person’s deci-
sion to have all the teeth removed, partial tooth
loss appears to be more closely related to oral
disease.14
For the same reasons as found for eden-
tulism, the sharpest improvement in reducing
tooth loss is evident in younger age-groups. As
an illustration of the extent of the improving
trend, in the first National Health and Nutrition
Examination Survey (NHANES I) of 1971-74,62
young people ages 12-17 years on average had
each lost 0.6 permanent teeth. Estimates from
the 1986-87 national survey of schoolchild-
ren,65 however, showed that average loss of per-
manent teeth in 12-17-year-olds had been
reduced to 0.05, a remarkable 12-fold decrease
over some 14 years.
The change is naturally not as sharp among
adults, because those adults who lost first
molars to caries when they were young will
continue to influence the data for a while yet.
However, comparison of data from the
NHANES I survey62 of 1971-74 with those from
the 1985-86 adult survey64 showed a sharp
improvement in tooth retention among den-
tate persons. In 1971-74, 59.5% of adults ages
18-74 had lost six or fewer teeth, whereas in
 19 Tooth Loss 227

60
White Mexican-American
African-American Other
50

40
Percent

30

20

10

0
25-34 35-44 45-54 55-64 65-74 75+

Age-group
Fig. 19-2 Proportion of the U.S. population edentulous by age and racial/ethnic group in the third National Health
and Nutrition Examination Survey, 1988-94.58

1985-86, 80.6% of employed adults ages 18-64
had lost six or fewer. Fig. 19-4 shows mean
tooth loss among U.S. adults in 1971-74, in
1985-86, and in the NHANES III survey of
1988-94. The bias toward higher SES of the
sample in the 1985-86 survey means that the
national extent of tooth loss projected from
that survey is most likely an underestimate; the
true extent of the improvement in tooth reten-
tion can be seen in comparing the 1971-74 data
with that from 1988-94. Tooth retention is
improving at all ages.
Fig. 19-5 shows the mean number of lost
teeth according to income level among dentate

60
Severe poverty
50 Medium
No poverty

40
Percent

30

20

10

0
25-34 35-44 45-54 55-64 65-74 75+

Age-group
Fig. 19-3 Proportion of the U.S. population edentulous by age and poverty status in the third National Health and
Nutrition Examination Survey, 1988-94.58
228 The Distribution of Oral Diseases and Conditions
16
1971-74
14 1985-86
1988-94
12
10
Mean tooth loss
0
18-24 25-34 35-44
Age-group
Fig. 19-4 Mean number of missing teeth in dentate adults and seniors in the United States, 1971-74, 1985-86, and
1988-94.58,61,64
adults in 1988-94. As was seen with edentulism,
income (which reflects SES) is an important risk
indicator for tooth loss. Also as with eden-
tulism, gender differences in partial tooth loss
have diminished. Fig. 19-6 shows the mean
number of teeth remaining in dentate men and
women as found in the NHANES III survey.
Longitudinal studies to identify risk factors
that lead to tooth loss, either total or partial,
have not been very successful.27,30 Smoking, not
surprisingly, has been identified as a risk indica-
tor,23,25,28,39 and early tooth loss was found to
be a strong predictor of subsequent eden-
tulism.23 SES in early life is also a demonstrated
predictor of tooth loss in early adulthood.56
REASONS FOR TOOTH LOSS
Conventional wisdom for many years was that
caries was the main reason for tooth loss before
age 35 and periodontal disease the main reason
after age 35. This belief was based on some
ancient and rather dubious data.11,51 The older
of these reports stated that “periclasia” was the
45-54 55-64 65-74 75+
main reason for tooth loss “after maturity.”
Even as late as 1978 there was a report that 8%-
10% of teeth are lost to periodontal disease by
age 40 and that such loss increases rapidly after
that age.38
Whether or not such historical views were
accurate, the picture has changed considerably.
From around the mid-1980s, studies in a num-
ber of countries and among different types of
populations have been consistent in finding that
caries is the principal cause of tooth loss at most
ages, with the possible exception of the oldest
(i.e., persons over 80 years).66 Data on which
these conclusions were based came from surveys
of practitioners,1,2,9,10,15,17,35 reviews of dental
records,6,16,48,55 and examinee questioning or
diagnosis during survey examinations.5,21,41,42,46
One exception to this trend was reported in
Canada, where an Ontario survey found that
periodontal diseases were the main reason given
for extraction of most teeth in patients over 40
years of age, although multiple extractions in a
relatively small number of patients can skew
such data.47 It is interesting to note that data
 19 Tooth Loss 229

14
Low income
12 Medium income
High income

10
Mean tooth loss

0
18-24 25-34 35-44 45-54 55-64 65-74 75+
Fig. 19-5 Mean number of missing teeth in dentate adults by income level and age in the United States, 1988-94.58

were published as long ago as 1944 showing that odontal diseases and 35% for caries. When the
most teeth were extracted for caries.3 patient was taken as the analytical unit, however,
A slight twist on this view came from a study 58% of patients had an extraction for caries and
of dental records of 1877 insured patients ages 40% for periodontal diseases.52 Caries tends to
40-69 years in the Kaiser Permanente health sys- result in extraction of one aching tooth, whereas
tem in the western United States. Of all teeth periodontal diseases (real or presumed) can lead
extracted in 1992, 51% were extracted for peri- to a treatment decision for a full clearance.

30
Female
Mean number of remaining teeth

25 Male

20

15

10

0
18-24 25-34 35-44 45-54 55-64 65-74 75+

Age-group
Fig. 19-6 Mean number of teeth remaining in dentate men and women by age in the United States, 1988-91.43
230 The Distribution of Oral Diseases and Conditions
DENTAL CARE AND TOOTH LOSS
At the risk of stating the obvious, it is worth
reminding ourselves that the main reason teeth
are lost is because dentists extract them. To
expand on that profound thought, “periodontal
disease” may have been the chief reason for
extraction in the era of “focal infection” (see
Chapter 1), because no doubt many teeth with no
more than severe gingivitis were extracted in the
name of periodontal disease. The reasons given
for the extractions were honest, but it seems likely
that in many cases the disease was probably not
what today would be considered severe. With the
better understanding of periodontal diseases now
prevailing, most such extractions have now
ended. There are two major reasons for continu-
ing improvement in tooth retention: (1) the
modern preventive philosophy governing dental
treatment, so that most present-day dentists
extract teeth only when there is no practical alter-
native; and (2) positive attitudes among today’s
adults, both younger and older. Tooth loss for
many of them is like smoking in the sense that
both are simply unacceptable.
In summary, tooth retention is improving
because of better prevention and control of the
oral diseases, more positive attitudes toward
tooth retention, and more conservative dental
treatment philosophies. The result is that the
proportion of people who are edentulous will
continue to diminish until it bottoms out,
probably at around 3%-4% of the population.
Dentate persons will continue to retain more
teeth as extractions for all reasons become less
common. The greater retention of teeth will
continue despite the aging of society, so the
older dentate patient will become more and
more common in dental practice.
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Canadian adult population. J Can Dent Assoc 1994;60:
549-55.
46. Mosha HJ, Lema PA. Reasons for tooth extraction
among Tanzanians. East Afr Med J 1991;68:10-4.
47. Murray H, Locker D, Kay EJ. Patterns of and reasons for
tooth extractions in general dental practice in Ontario,
Canada. Community Dent Oral Epidemiol 1996;24:
196-200.
48. Niessen LC, Weyant RJ. Causes of tooth loss in a veteran
population. J Public Health Dent 1989;49:19-23.
49. Nizel AE, Bibby BG. Geographic variations in caries
prevalence in soldiers. J Am Dent Assoc 1944;31:
1619-26.
50. Osterberg T, Carlsson GE, Sundh W, Fyhrlund
A. Prognosis of and factors associated with dental status
in the adult Swedish population, 1975-1989. Commu-
nity Dent Oral Epidemiol 1995;23:232-6.
51. Pelton WJ, Pennell EH, Druzina A. Tooth morbidity
experience of adults. J Am Dent Assoc 1954;49:439-45.
52. Phipps KR, Stephens VJ. Relative contribution of caries
and periodontal disease in adult tooth loss for an
HMO dental population. J Public Health Dent 1995;
55:250-2.
53. Schlack CA, Restarski JS, Dochterman EF. Dental status
of 71,015 naval personnel at first examination in 1942.
J Am Dent Assoc 1946;33:1141-6.
54. Steele JG, Walls AW, Ayatollahi SM, Murray JJ. Major
clinical findings from a dental survey of elderly people
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1996;180:17-23.
55. Stephens RG, Kogon SL, Jarvis AM. A study of the rea-
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56. Thomson WM, Poulton R, Kruger E, Boyd D. Socio-eco-
nomic and behavioural risk factors for tooth loss from
age 18 to 26 among participants in the Dunedin
Multidisciplinary Health and Development Study.
Caries Res 2000;34:361-6.
57. Todd JE, Whitworth A. Adult dental health in Scotland,
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58. US Department of Health and Human Services,
National Center for Health Statistics. Third National
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Public Use Data File No. 7-0627. Hyattsville MD:
Centers for Disease Control and Prevention, 1997.
59. US Public Health Service. Loss of teeth, United States
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Series B No. 22. Washington DC: Government Printing
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60. US Public Health Service, Centers for Disease Control
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19, 2003.
61. US Public Health Service, National Center for Health
Statistics. Edentulous persons, United States 1971.
DHEW Publication No. (HRA) 74-1516, Series 10 No.
89. Washington DC: Government Printing Office, 1974.
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62. US Public Health Service, National Center for Health
Statistics. Decayed, missing, and filled teeth among per-
sons 1-74 years; United States. DHHS Publication No.
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Government Printing Office, 1981.
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2003.
 20 Dental Caries
GLOBAL DISTRIBUTION OF CARIES
SECULAR VARIATIONS IN CARIES
EXPERIENCE
UNEVEN DISTRIBUTION OF CARIES
REGIONAL VARIATIONS IN CARIES
DISTRIBUTION IN THE UNITED STATES
CARIES DISTRIBUTION: DEMOGRAPHIC RISK
FACTORS
Age
Gender
Dental caries is an ancient disease, dating back
to at least the time that agriculture replaced
hunting and gathering as the principal source of
food. Examination of skulls in Britain suggests
that the moderate caries experience found in the
Anglo-Saxon period (fifth to seventh centuries)
had changed little by the end of the Middle
Ages, approximately the year 1500.154,155
Dental attrition in this period was extensive and
occurred early in life; some lesions in young
persons seem to have begun in the occlusal fis-
sures but developed no further because attrition
progressed faster than caries. Most lesions
found in human remains from this period were
cervical or root caries; coronal caries was rela-
tively uncommon. The modern pattern of caries
in the high-income nations, with lesions begin-
ning in fissured surfaces and developing later
on proximal surfaces, was not evident in Britain
until the sixteenth century.156
Dietary changes that began during the eigh-
teenth century, principally increased refinement
of foods and greater availability of sugar, are
considered chiefly responsible for the develop-
ment of the modern pattern of caries. Import
duties on sugar in Britain were relaxed in 1845
and completely removed by 1875, a period dur-
ing which the severity of caries greatly
Race and Ethnicity
Socioeconomic Status
Familial and Genetic Patterns
CARIES DISTRIBUTION: RISK FACTORS AND
RISK INDICATORS
Bacterial Infection
Nutrition and Caries
Diet and Caries
ROOT CARIES
EARLY CHILDHOOD CARIES
increased.51,119 By the end of the nineteenth
century, dental caries was well established as an
endemic disease of massive proportions in
most developed countries.35
This chapter examines the distribution of
dental caries in populations and the factors that
influence that distribution. Although there is a
rare disease known as bone caries, we use the
term caries in this chapter to refer to dental
caries.
GLOBAL DISTRIBUTION OF CARIES
Although some of the historic patterns of high
attrition, little coronal caries, and moderate
prevalence of root caries could still be found in
remote places in the twentieth century,184-186
they are fast disappearing as once-isolated pop-
ulations become infected with cariogenic bacte-
ria and increasingly adopt the cariogenic diets
and lifestyles of the developed world.
For most of the twentieth century, caries was
seen as a disease of the high-income countries,
with low prevalence in poorer countries. The
most obvious reason for this pattern is diet. The
high level of consumption of refined carbohy-
drates in the wealthier countries led to selective
proliferation of cariogenic bacteria.52 Poorer
233
234 The Distribution of Oral Diseases and Conditions

societies, on the other hand, survived by hunt-
ing and subsistence farming, both of which pro-
vided diets low in fermentable carbohydrates.
By the late twentieth century, there were signs
of change in this traditional pattern. First, there
was some evidence that caries experience in
some low-income countries had risen sharply
in the years after World War II (1939-45).151
However, this change was by no means univer-
sal, and caries incidence in many such coun-
tries, especially those in Africa, remains
relatively low.12,50,144,158-160 The second change
is the marked reduction in caries experience
among children and young adults in high-
income countries, a trend that first became evi-
dent in the late 1970s.35 This change, which has
already had a marked impact on dental practice,
will affect oral conditions among the whole
population in due course as today’s younger
cohorts progress through the life span.
The World Health Organization (WHO)
maintains the Global Oral Health Data Bank, a
collection of surveillance data from almost all
countries in the world. The most extensive data
set in the data bank is for DMFT values (num-
ber of decayed, missing, or filled permanent
teeth) for 12-year-olds, a response to the global
goal set by WHO in 1982 (see Chapter 5). Table
20-1 shows the trends in these values in 11
high-income countries over a recent period of
some 10-20 years. In most of these countries the
decline in caries levels has been substantial,
even spectacular in some cases. It is not univer-
sal, however, because both Korea and Kuwait
have seen a rise in DMFT scores. This could be
because preventive measures have lagged
behind growing affluence in these two coun-
tries, whereas preventive measures have
become established, at least to some extent, in
the other nine.
Table 20-2 shows the same trends for middle-
income countries, those without the resources
of the countries in the previous table, and here
the pattern is different. Only Cuba, which has
had a school dental service for years, and
Estonia, where caries levels were very high, have
shown a substantial drop in caries levels over
the same 10-20 years. Of the others, four have
shown a minor decline, and four have had an
increase. These countries are arbitrarily chosen
from many in WHO’s Global Oral Data Bank,
but they do show a picture that is fairly repre-
sentative—nations with better-developed pub-
lic health prevention generally have shown
most success in caries prevention. However,
among countries of all income levels there are
distinct differences in caries experience from
one country to another, and from region to
region within a country. Intercountry differ-
ences are illustrated by the results of the first
International Collaborative Study (ICS I), pro-
moted by WHO with funding and cooperation
from the U.S. Public Health Service and the par-
ticipating countries. These data were collected
during the mid-1970s,9 and the mean DMFT
values for children ages 13-14 in the first seven

Table 20-1 Trends in dental caries experience, as measured by mean DMFT values in 12-year-old children, in 11
high-income countries* in the late twentieth century233
Country Initial DMFT Latest DMFT Initial Year Latest Year

Australia 3.0 0.8 1982 1999

Denmark 5.0 0.9 1980 2001
Finland 4.0 1.1 1982 1997
France 4.2 1.9 1987 1998
Iceland 8.3 1.5 1982 1996
Ireland 3.3 1.3 1984 2002
Korea 2.5 3.1 1979 1995
Kuwait 2.0 2.6 1982 1993
Japan 5.4 2.4 1981 1999
Spain 4.2 2.3 1984 1994
USA 1.8 1.3 1987 1994
*Asdefined by the World Bank in World Bank Group, Data and statistics, Country groups, website: http://www.worldbank.org/data/
countryclass/classgroups.htm. Accessed December 18, 2003.
 20 Dental Caries 235

participating countries are shown in Fig. 20-1.
These data were not from nationally representa-
tive population samples but rather from
selected communities. The data for the United
States, for instance, came from the metropolitan
area of Baltimore, a city with fluoridated water
since 1952. The areas chosen for examination in
Australia (Sydney) and Canada (Ontario) also
had had fluoridated water for some years.
The data in Fig. 20-1 provide some food for
thought regarding both caries treatment and its
measurement. The two highest mean DMF val-
ues are found in Norway (Trøndelag) and New
Zealand (Canterbury), both countries with
extensive school dental services. The same two
countries, it will be noticed, have the lowest
mean D values, virtually no tooth loss, and by
far the highest mean F values. As noted in the

Table 20-2 Trends in dental caries experience, as measured by mean DMFT values in 12-year-old children, in 11
lower-middle- and upper-middle-income countries* in the late twentieth century233
Country Initial DMFT Latest DMFT Initial Year Latest Year

China 0.8 1.0 1983 1996

Cuba 2.9 1.4 1989 1998
Estonia 4.1 2.7 1992 1998
Lithuania 3.6 4.9 1986 1994
Malaysia 2.4 1.6 1988 1997
Morocco 2.3 2.5 1991 1999
Poland 4.4 3.8 1985 2000
Saudi Arabia 2.0 1.7 1985 1995
Sri Lanka 1.9 1.4 1984 1995
Thailand 1.5 1.6 1984 2001
Trinidad Tobago 4.9 5.2 1989 1998
*As defined by the World Bank in World Bank Group, Data and statistics, Country groups, website: http://www.worldbank.org/data/coun-
tryclass/classgroups.htm. Accessed December 18, 2003.

14
Filled

12 Missing

Decayed
10
Mean DMFT

0
Sydney Trondelag Canterbury Hannover Yamanashi Baltimore Ontario
Fig. 20-1 Decayed, missing, and filled permanent teeth in children ages 13-14 in seven countries. Data from the first
International Collaborative Study, 1973-75.15,25,67
236 The Distribution of Oral Diseases and Conditions
discussion of the DMF index in Chapter 15,
data such as those in Fig. 20-1 reflect dental
treatment as much as disease.
SECULAR VARIATIONS IN CARIES
EXPERIENCE
When caries was more prevalent and severe
than at present, affected teeth were attacked
within 2-4 years after eruption. By the early
1980s, there were reports from local surveys to
suggest that the average prevalence and severity
of caries among children in the United States
was declining from its previously high lev-
els.34,72,87,200 Similar information from other
high-income countries around the same
time7,88,89,143,182 indicated that this reduction
in caries experience was widespread.
The decline in caries experience among chil-
dren was confirmed for the United States by
results of the National Dental Caries
Prevalence Survey of U.S. schoolchildren in
1979-80.219 This survey showed that mean
DMF scores among children ages 5 to17 years
were some 32% lower than those found in the
first National Health and Nutrition
Examination Survey (NHANES I) of 1971-
74.217 The next national survey of U.S. school-
children in 1986-87 found that the decline was
continuing,221 with mean DMF scores for 5- to
12
Filled
10 Missing
Decayed
8
Mean DMFS
0
9 11
Age in years
Fig. 20-2 DMFS values for U.S. children ages 9-17, in 1979-80 and 1988-94.213,219
17-year-olds again 36% lower than those from
7 years earlier, and further decline was seen in
the third National Health and Nutrition
Examination Survey (NHANES III) of 1988-
94.213 Mean DMFS scores (number of decayed,
missing, or filled permanent tooth surfaces) for
schoolchildren ages 9-17 in 1979-80 and
1988-94 are shown in Fig. 20-2, and the reduc-
tion in caries experience is obvious. In the
1988-94 data there were few missing teeth, and
the highest mean value for decayed surfaces
was 1.14 for the 17-year-olds. The index bars
for 1988-94 data in Fig. 20-2 are made up pre-
dominantly of the F component. The decline
has also been documented in primary teeth:
mean dfs scores (number of decayed or filled
primary tooth surfaces) for 6-year-olds in the
1979-80 survey was 4.76;219 this was down to
3.73 in 1986-87.221
The seemingly sudden caries decline among
children in high-income nations was docu-
mented at a conference in Boston in 1982, the
proceedings of which were published in a
special issue of the Journal of Dental Research in
November 1982. The caries decline in the
permanent dentition among children of high-
income nations has continued since
then,10,23,37,47,56,117,140,195,211 although caries
experience in the primary dentition may have lev-
eled out by the early 1990s.33,37,79,98,140,194,211
1979-80 = Left columns
1988-94 = Right columns
13 15 17

Although the downward trend in caries experi-
ence (permanent teeth) among American and
Canadian children was continuing through the
1990s, the rate of decrease must get slower as
overall caries experience approaches an irre-
ducible minimum level. The main caries problem
in the United States and some other countries
today is not so much overall caries levels as the
disparities in disease experience and treatment
between different socioeconomic and racial-
ethnic groups.
The reduction in caries has not occurred
evenly for all kinds of tooth surfaces; it has
been proportionately greater for free smooth
surfaces and proximal surfaces than for pit-
and-fissure surfaces.24,110,196 An unexpected
outcome in a 3-year longitudinal study in
Michigan in the early 1980s was that 81% of all
new lesions were on pit- and-fissure surfaces.
No lesions at all were found on free smooth
surfaces.38
As caries prevalence falls, the least susceptible sites
(proximal and smooth surfaces) reduce by the greatest pro-
portion, while the most susceptible sites (occlusal) reduce
by the smallest proportion.142
The net result is that, although the total num-
ber of new carious lesions has been declining,
an increasing proportion of them is made up of
pit- and-fissure lesions. This trend has
enhanced the attractiveness of fissure sealants
as a preventive measure (see Chapter 27).
History has many examples of diseases that
have waxed and waned without precise knowl-
edge of why, and the caries decline is one
of these. No clear reasons for the caries
decline have been identified, although most
researchers view the various uses of fluoride as
the main cause.30 Sugar consumption in the
United States has increased (see Chapter 28)
rather than diminished, and it is difficult to
ascribe the decline to better oral hygiene or to
changes in the bacterial ecology of the oral cav-
ity, whereas an influential role for fluoride is
hard to reject.36 Even the effect of widespread
use of pediatric antibiotics on oral bacteria has
been suggested as a contributory factor.128
However, as with other diseases that show
a cyclical nature over time, it is quite likely
that factors are operating that have not been
identified.
20 Dental Caries 237
UNEVEN DISTRIBUTION OF CARIES
For many years, the results of surveys and even
research studies were presented only as mean
DMF values, usually with only a standard devia-
tion to indicate the distribution. Although
means are useful, they compress extreme values
(i.e., absence of caries and caries in many teeth
in the same mouth) into an average figure that
sometimes can be misleading. A landmark
break from this convention came with the
results of the National Preventive Dentistry
Demonstration Program (NPDDP) in the mid-
1980s. The NPDDP studied the effects of a
series of preventive procedures in children in
grades 1, 2, and 5 in five cities with and five
cities without fluoridated water. The NPDDP
drew attention to the fact that, although average
caries experience in children was lower than the
researchers had originally expected, there was
still a significant minority with severe caries.74
This type of distribution is illustrated in Fig. 20-3,
which provides data from the national surveys
of schoolchildren in 1979-80 and 1988-94.
Whereas Fig. 20-2 illustrates the decline in mean
DMFS scores that occurred between the two sur-
veys, Fig. 20-3 shows the distributional changes.
It is evident that in the more recent survey the
proportion of “caries-free” children (Box 20-1)
had increased, whereas the proportion with
severe caries had decreased. Even so, the shape
of the distribution remained much the same:
highly skewed toward zero or few DMFS teeth,
but with a persistent “tail,” meaning that there
were still children at the severe end of the scale.
Although there is no established definition
of “severe” caries, DMFS values of 7.0 or higher
today can be considered to indicate severe dis-
ease in children up to age 17. Of all U.S. chil-
dren, 27.3% fell into this category in 1979-80;
this number had dropped to 17.3% by 1986-87.
To pick a round figure, 20% is a fair estimate of
the proportion of U.S. children who suffer from
severe caries.
Fig. 20-4 is a cumulative frequency curve
demonstrating that most caries occurs in a rela-
tively small number of children. This figure is
restricted to children of the same age (in this
case, 15 years) so that the curve does not reflect
age differences. When the values in Fig. 20-4 are
read off, it can be seen that 60% of all affected
238 The Distribution of Oral Diseases and Conditions

60
1979-80
1988-94
50

40
Percent

30

20

10

0
0 1-3 4-6 7-9 10-12 13+

Mean DMFS
Fig. 20-3 Distribution of mean DMFS values in U.S. schoolchildren ages 5-17, 1979-80 and 1988-94.213

BOX 20-1 What Does Caries Free Mean?

The term caries free has traditionally been used to describe people with a DMF score (number of decayed, missing, or
filled teeth) of 0, usually when the presence of a dentinal, or D3, lesion is the stated or implied criterion for caries. As
the understanding of caries has increased, it has become evident that very few people are literally caries free. Just
about everyone, at any given time, has some level of carious activity taking place. Most of this activity consists of early
demineralization-remineralization cycles or a white spot or stained fissure that does not progress. In a healthy mouth,
the bulk of this activity does not reach the stage where restorative dental treatment is needed, although preventive
intervention may be called for. But this still means that the term caries free is not correct. Perhaps more importantly,
use of this term can tend to promote a mindset that caries does not matter, or perhaps does not even exist, until it
involves the dentin. That is clearly incorrect, for preventive treatment at this stage can forestall the need for later
restorative treatment. A more accurate term would be free of caries requiring restorative treatment, but that is much
too clumsy for everyday use.
The term caries free will continue to be used in this context because it has history and ease of use on its side. It
must be remembered, however, that rarely is it a strictly correct term. It is used to mean that caries has not reached a
stage where operative dental treatment is needed.

teeth are found in about 20% of children, and

three fourths of all affected teeth are found in
about one fourth of the children. This concen-
tration of disease in relatively few children has
led to the concept of targeting public health pre-
vention programs toward that highly affected
minority, and it has stimulated research into
methods of predicting which children are likely
to be in the 20% or so that is most affected (see
Chapter 14).
REGIONAL VARIATIONS IN CARIES
DISTRIBUTION IN THE UNITED STATES
Regional variations in caries experience within
the United States were first documented with
the examination of young men in the armed
forces during World War II.104,164,188,190 It is of
interest to note that regional differences in
caries prevalence among different tribes of
Native Americans were demonstrated in the
 20 Dental Caries 239

100
Cumulative percent of total DMFS

80

60

40

20

0
0 10 20 30 40 50 60

Cumulative percent of children 15 years old

Fig. 20-4 Cumulative frequency curve of the proportion of total DMF teeth in U.S. schoolchildren ages 15 years,
1988-94.213

early 1930s, 106 with more severe disease CARIES DISTRIBUTION:

among tribes in the Northwest than among DEMOGRAPHIC RISK FACTORS
those in the Southwest. This regional pattern is
still seen today in the general American Age
population. Mean DMF scores increase with age, as shown
The World War II surveys were in general in Fig. 20-2 for schoolchildren and Fig. 20-6 for
agreement that the most severe caries experi- adults. It can be seen that the increase with age
ence was seen in recruits from New England, for the children’s’ cohorts comes largely from
the Pacific Northwest, and the Great Lakes an increase in numbers of restored teeth,
area, with distinctly less caries in young men whereas for the adults (see Fig. 20-6) most of
from the South, the Southwest, and the the increase with age comes from missing
mountain states. In the years since World War teeth. Both figures are from cross-sectional
II, some of these differences have been data, so as younger cohorts replace today’s
obscured by the spread of water fluoridation, older people, the M component will decrease
but they were still apparent in the late (see Chapter 19). With fewer restorations now
1960s.130 The regional differences in a repre- also being placed in younger people,60 the
sentative sample of youths ages 12-17 years in overall DMF values in older people are also
a national survey conducted in 1966-70 are likely to decline with time. The impact of the
illustrated for whites and African-Americans caries decline naturally takes longer to become
in Fig. 20-5. evident in adults than in children, because
Regional differences in caries experience many of those who were adults when the data
are not unique to the United States, for just in Fig. 20-6 were collected had already experi-
about every country exhibits similar enced much of their caries activity before the
variations. For example, in Britain, despite an modern age of prevention.
overall decline in caries experience that Caries used to be considered a childhood
parallels that seen in the United States, chil- disease, a perception that arose in days of high
dren’s oral health is still poorer in Scotland caries severity when most susceptible surfaces
and northern England than in southern were usually affected by adulthood. With
England.170,171 younger people now reaching adulthood with
240 The Distribution of Oral Diseases and Conditions

10

Filled
Missing
8
Decayed

6
Mean DMFT

0
W AA W AA W AA W AA
Northeast Midwest South West
Fig. 20-5 Decayed, missing, and filled permanent teeth in white (W) and African-American (AA) children ages 12-17
in four geographic areas of the United States, 1966-70.216

many surfaces free of caries, the carious attack is
spread out more throughout life. Adults of all
ages can develop new coronal lesions,57,77 and
caries has to be viewed as a lifetime disease.
Even the disease distribution seen in youth—
that is, the clustering of most disease in a rela-
tively small number of people (see Fig. 20-4)—is
seen in the elderly.145
In populations in which caries experience is
severe, the disease starts early in life and is com-

100
Filled
Missing
80
Decayed
Mean DMFS

60

40

20

0
15-24 25-34 35-44 45-54 55-64 65-74 75+

Age-group
Fig. 20-6 Mean DMFS values by age for U.S. adults, 1988-94.213

mon in the young. A more even occurrence of
new lesions throughout life is characteristic of
communities with a lower attack rate.
Gender
Females have usually demonstrated higher
DMF scores than do males of the same
age,215,220,221 although this finding is not uni-
versal. When observed in children, the differ-
ence has been attributed to the earlier eruption
of teeth in females,108,207 but this explanation is
hard to support when the differences are seen in
older age-groups. In those instances a treatment
factor is more likely to be contributing to the
differences. In national survey data, males usu-
ally have more untreated decayed surfaces than
females, and females have more restored teeth.
Females visit the dentist more frequently (see
Chapter 2), so this observation is perhaps to be
expected. In NHANES III, females ages 12-17
years had the same mean number of decayed
and missing surfaces as their male counterparts
but 25% more filled surfaces.98 We cannot con-
clude from these figures that females are more
susceptible to caries than are males; a combina-
tion of earlier tooth eruption plus a treatment
factor is a more likely explanation for the
observed differences.
Race and Ethnicity
Long-held contentions that certain races enjoy
a high degree of resistance to dental caries
probably came with early observations that
some non-European races, such as those in
Africa and India, enjoyed a greater freedom
from caries than did Europeans. Today, how-
ever, we accept that global variations in caries
experience result more from environment than
from inherent racial attributes. To illustrate that
point, there is evidence that certain racial
groups once thought to be resistant to caries
quickly developed the disease when they
migrated to areas with different cultural and
dietary patterns.17,152,179 In the United States,
most surveys before the 1970s found that
whites had higher DMF scores than African-
Americans, although the latter usually had
more decayed teeth because of poorer access to
care. The National Health Survey of 1960-62
showed that whites had higher DMF scores
than did African-American adults of the same
age-group, a difference that remained even
20 Dental Caries 241
when the groups were standardized for income
and education.214 Fig. 20-5, showing regional
differences in caries severity, also illustrates the
differences in DMF status between whites and
African-Americans in the 1960s. It can be seen
in Fig. 20-5 that overall DMF scores are higher
among whites, although big differences in den-
tal treatment are obvious. This difference was
still evident in NHANES I in 1971-74,217
although other studies from around that time
were finding little difference in DMF scores
between whites and African-Americans of the
same age.13,85
By the time of NHANES III in 1988-94,
however, there was little difference in total
DMF scores between whites and African-
Americans, although whites still had a higher
filled component and lower scores for decayed
and missing surfaces. Fig. 20-7 shows data for
children ages 13, 15, and 17 for illustration.
DMF values for Mexican-Americans were in the
midrange, and those in the “Other” racial-eth-
nic category had the highest overall DMF
scores of all. This turnaround could indicate
improving access to care for African-
Americans, although it most likely reflects
socioeconomic differences: the caries decline,
as previously noted, is sharpest in the higher
socioeconomic groups. The summary of rela-
tive DMFT scores for 12- and 15-year-old white
and African-American children in five national
surveys given in Fig. 20-8 illustrates the relative
changes down the years.
The caries status of Hispanic Americans has
not been as well studied, although valuable
information came from the Hispanic Health
and Nutrition Examination Survey (HHANES)
of 1982-84. Data showed that DMF scores of
Mexican-American adults were lower than the
national average, but the D component was
higher.90 Among children, a similar picture
emerged in Mexican-Americans of the
Southwest, Cuban communities of Miami, and
Puerto Rican groups in New York.92
The overall pattern gives no reason to believe
that inherent differences exist in caries suscepti-
bility among African-Americans, people of
Hispanic origin, and whites. Socioeconomic
differences—that is, differences in education,
self-care practices, attitudes, values, available
income, and access to health care—appear to be
far more important.
242 The Distribution of Oral Diseases and Conditions

9
Filled
8 Missing
Decayed
7

6
Mean DMFS

0
W AA MA O W AA MA O W AA MA O
13-year-olds 15-year-olds 17-year-olds
Fig. 20-7 Mean DMFS values for 13-, 15-, and 17-year-old children in white (W), African-American (AA), Mexican-
American (MA), and other (O) racial and ethnic groups in the United States, 1988-94.213

White
African-American
White
African-American
8

6
Age 15
5
Mean DMFT

Age 12
3

0
1966-70 1971-74 1979-80 1986-87 1988-94
Years of survey
Fig. 20-8 Mean DMFT scores for 12- and 15-year-old white and African-American children in five national surveys
in the United States, 1966-70 to 1988-94.213

Socioeconomic Status
Socioeconomic status (SES), called social class in
Britain, is a broad recording of an individual’s
attitudes and values as measured by such factors
as education, income, occupation, and place of
residence. Attitudes toward health are often part
of the set of values that follow from an individ-
ual’s prestige in society and may explain some
of the observed differences in health between
SES groups. However, obtaining a valid measure
of SES is always a problem because of its com-
plexity. In the United States SES is usually meas-
ured by annual income or years of education,
despite acknowledged shortcomings in these
measures.76
SES is inversely related to the incidence of
many diseases and to characteristics thought to
affect health.136 The reasons seem obvious in
many cases, but not all.123 For example, differ-
ences in infant mortality by SES can be explained
partly by the fact that higher SES women have
better access to prenatal care, more ability to
afford such care, the time to get it, probably less
fatalistic attitudes, and perhaps some other fac-
tors.68 However, even after all these likely vari-
ables have been factored into explaining the
differences, there is still a considerable gap that
defies explanation. In dental health, a similar
finding was reported in Finland,148 where differ-
ences in caries experience between children in
the higher and lower social classes still remained
after accounting for age, sex, reported frequency
of toothbrushing, consumption of sugars, and
ingestion of fluoride tablets. Children in Finland
also have virtually equal access to publicly
funded dental care, regardless of SES, which is
not the case in the United States. Measurements
used in science cannot always pick up all the sub-
tleties embedded in SES.
As part of his landmark research in caries epi-
demiology during the 1930s and 1940s, Klein
observed that overall DMF values did not differ
between SES groups, but aspects of treatment
certainly did.109 Lower SES groups had higher
values for D and M, and lower values for F. In the
first national survey of U.S. children in 1963-65,
white children in the higher SES strata actually
had higher DMF scores than did white children
in the lower strata, but African-American chil-
dren showed the opposite pattern.215 In both
white and African-American children, the mean
20 Dental Caries 243
number of D teeth diminished with increasing
SES, and the mean number of M teeth showed
little change. In white children, however the F
component ballooned so much with increasing
SES that it lifted the whole DMF index. By con-
trast, the F component in the African-American
children did not change, with the net result that
DMF diminished with increasing SES. As men-
tioned earlier, these results from 1963-65
showed that a “treatment effect” (see Chapter
15) was artificially inflating the DMF data in the
white children, whereas the values for the
African-American children were likely to be a
more valid measure of the carious attack.
With the lower overall caries experience of
today, however, the position has been reversed.
The NPDDP showed that the higher SES groups
have enjoyed the sharpest decline in caries expe-
rience,74 so that the DMF values of children in
the higher SES strata are now considerably below
those of children in the lower SES strata. This is
illustrated in Fig. 20-9, which graphs the compo-
nents of the DMFS index for 15-year-old children
in low, medium, and high SES groups as meas-
ured in NHANES III in 1988-94. Fig. 20-10 shows
the same components for adults in three age-
groups, and the same patterns can be seen rela-
tive to SES. Among the older adults, those in the
higher SES groups had fewer missing and more
filled surfaces. In the younger group, however,
both total DMFS scores and the values of all of its
components were lower in the higher SES
groups. These data in Fig. 20-10 suggest that there
may be a treatment effect in older age-groups
that grew up before the preventive era, but
among the 15- to 24-year-olds the higher SES
groups clearly have lower caries experience.
Relationships between caries status and a
broad range of SES measures (e.g., residence in
private versus public housing, car ownership,
quality of neighborhoods) have also been
reported in Britain44-46,73,166 and elsewhere in
Europe.83,141 When measures of social status
appropriate for a nonindustrialized society have
been used, such patterns have also been
observed in Africa.146 The British studies noted
that, although fluoridation of water supplies
(see Chapter 25) reduces the difference between
the social classes, it does not entirely remove it.
These studies collectively demonstrate that
dental caries today can be looked upon as a
244 The Distribution of Oral Diseases and Conditions

6
Filled
Missing
5
Decayed

4
Mean DMFS

0
Low Middle High
Socioeconomic status groups
Fig. 20-9 Mean DMFS scores for 15-year-old children at three socioeconomic levels in the United States,
1988-94.213

80
Filled
Missing
Decayed
60
Mean DMFS

40

20

0
Low Medium High Low Medium High Low Medium High
15-24 years 35-44 years 55-64 years

Socioeconomic status and age-group

Fig. 20-10 Mean DMFS scores in adults ages 15-24 years, 35-44 years, and 55-64 years at three socioeconomic
levels in the United States, 1988-94.213

disease of poverty or deprivation. The greatest
reductions in caries experience have been
enjoyed by the upper social groups, whereas
reductions in the lower social groups have been
more modest. When treatment programs are
planned, caries experience can be expected to be
more extensive and severe among lower SES
populations.
Familial and Genetic Patterns
Familial tendencies (“bad teeth run in families”)
are noted by many dentists and have been clearly
demonstrated.70,107,111,174 However, these studies
do not pin down whether such tendencies have a
genetic basis or whether they stem from bacterial
transmission or continuing familial dietary or
behavioral traits. Husband-wife similarities
clearly have no genetic origin, and intrafamilial
transmission of cariogenic flora, especially from
mother to infant, is accepted as a primary way for
cariogenic bacteria to become established in chil-
dren.113,114,175 The lack of a genetic influence by
race, discussed earlier, weakens the case for
genetic inheritance of a susceptibility or resist-
ance to caries, although Klein concluded that the
similarities within families involved “strong
familial vectors which very likely have a genetic
basis, perhaps sex-linked.”105 Studies of identical
twins have concluded that, although genetic fac-
tors could have affected caries experience to
some extent, the influence of environmental
variables was stronger.135
With the explosion of research discoveries of
genetic influences in many diseases, dental
caries is being viewed in a different light. It is
likely that host attributes which could affect an
individual’s caries experience, such as salivary
flow and composition, tooth morphology, and
arch width, are genetically determined, and the
genetics of the cariogenic bacteria themselves
must have an effect. The rapid growth of
research technology and interest in genetics
holds promise that a new view of caries will
emerge in the future.
CARIES DISTRIBUTION: RISK
FACTORS AND RISK INDICATORS
Many factors are considered to be part of the
causal web in dental caries: bacteria, diet,
plaque deposits, saliva quantity and quality,
enamel quality, and tooth morphology have all
20 Dental Caries 245
been so considered. We do not attempt to detail
the role of all of these factors in caries develop-
ment; instead the reader is referred to texts such
as Dental caries: the disease and its clinical man-
agement.63 However, the role of bacteria and
diet as risk factors (according to the definition
given in Chapter 13) for development of caries
is worth considering here.
Bacterial Infection
Caries is a bacterial disease. Bacteria are a neces-
sary condition for its occurrence; that is, regard-
less of any other factor, caries cannot occur in
the absence of bacteria.62,127 The bacteria princi-
pally involved, the mutans streptococci and lac-
tobacilli, are normal constituents of the flora in
most mouths, so in that sense caries can be seen
as an ecologic imbalance rather than an exoge-
nous infection. It has been described as a carbo-
hydrate-modified bacterial infectious disease, in
which a cariogenic diet selectively favors cario-
genic bacteria.223 Cariogenic bacteria are trans-
missible, usually passed along from mother to
child.114,116,175 The complexity of bacterial inter-
actions in caries development is illustrated by
the finding that establishment of Streptococcus
sanguinis during a “window of infectivity” in an
infant appears to be antagonistic to the colo-
nization of Streptococcus mutans.48
When caries experience is studied in groups,
it usually is inversely related to counts of
mutans streptococci in saliva or plaque,20,26,112
although this relationship is not strong. At the
individual level, however, bacterial counts by
themselves are a poor predictor of future
caries.3,81,192 Although negative predictive val-
ues can be high (i.e., low bacterial counts pre-
dict the nondevelopment of caries fairly well),
positive predictive values are not (i.e., high bac-
terial counts do not predict the development of
future caries).101
The evidence is not yet clear enough to per-
mit quantification of the risk attributable to
specific bacteria, which in any case may vary in
different populations. However, because infec-
tion with cariogenic bacteria is a necessary con-
dition for caries to occur, it is obviously a risk
factor for caries.
Nutrition and Caries
The term diet refers to the total oral intake of
substances that provide nourishment and
246 The Distribution of Oral Diseases and Conditions
energy, whereas nutrition refers to the absorp-
tion of nutrients. In view of nutrition’s funda-
mental role in human health, it is natural that
its etiologic function in caries should have
received a lot of attention. The suggestion that a
deficiency of vitamin D is a causative factor in
subsequent hypoplasia and development of
dental caries147 dates from 1934 and was most
likely influenced by contemporary findings on
vitamin-deficient diseases. There is evidence
from studies of children in Peru that chronic
and severe malnutrition during the first year of
life is associated with increased caries years
later, although this association is difficult to
demonstrate because malnutrition delays erup-
tion and exfoliation of the primary teeth.5
Chronic malnutrition among children in India
has been shown to reduce salivary flow, which
could be one reason for a causative link.94
The epidemiologic evidence shows that,
before the development of modern preventive
methods, the prevalence of caries was lowest in
those countries in which living standards were
also lowest: even where generalized malnutri-
tion was the norm, dental caries was uncom-
mon.1,58,133,139,178-180,206 This pattern is
unlikely to have arisen because of protective fac-
tors in the unprocessed diet in poor societies,
for it is very hard to identify any such factors
that actually function in humans.27 It is far
more likely that the observed pattern came from
nonexposure to the cariogenic foods found in
high-income countries. Even in those countries
in which caries prevalence is rising, this increase
is largely confined to urban populations in
which both dietary and cultural changes are
occurring rapidly. Traditional village popula-
tions in Africa still show little sign of dental
caries, although many of them suffer from some
degree of malnutrition.2,12,50,151,158-160,165,182
In the United States, no relation between nutri-
tional adequacy and DMF scores could be
found in NHANES I in 1971-74.218
The limited epidemiologic evidence thus
favors the conclusion that severe, chronic mal-
nutrition during infancy can predispose peo-
ple to later dental caries. This situation is
found in countries where malnourishment
during early childhood is common but where
there is later exposure to cariogenic foods; the
malnutrition itself does not produce caries
without the later cariogenic challenge. In the
high-income nations, this degree of severe
malnutrition is rare and is seen only in highly
unusual circumstances.
Diet and Caries
In contrast to nutrition, diet has a clear influ-
ence on caries development. In particular, the
relation between the intake of refined carbohy-
drates, especially sugars, and the prevalence
and severity of caries is so strong that sugars are
clearly a major etiologic factor in the causation
of caries. This link has been recognized for
many years.29,39,64,131,161,162,176,191 Added sug-
ars are the primary culprit, although a limited
degree of caries occurs in populations for
whom the only sugars consumed are naturally
occurring.183
Although the evidence that consumption of
sugars is a major risk factor for caries can be
described as overwhelming, sugars are not the
only food sources involved in the carious
process. Cooked or milled starches can be bro-
ken down to low-molecular-weight carbohy-
drates by the salivary enzyme amylase and thus
act as a substrate for cariogenic bacteria. It has
been asserted that sugar-starch mixtures are
more cariogenic than sugars alone,22 and there
is some animal evidence to support that view.65
The issue may never be totally clarified in
humans, but it is reasonable and prudent to
view all sugar-containing food and drinks, as
well as cooked or milled starches, as potentially
cariogenic. By contrast, the high-molecular-
weight carbohydrates in lightly cooked vegeta-
bles are considered noncariogenic because so
little breakdown of these foods occurs in the
mouth.115,163
Early Theories on Diet and Caries
The great exploratory voyages of the seven-
teenth and eighteenth centuries led to the dis-
covery of peoples previously unknown to
Europeans, such as the islanders of the South
Pacific, who appeared to live an idyllic life free
of the diseases that afflicted Europe at the time.
The concept of the “noble savage”59 thus devel-
oped during the latter part of the eighteenth
century. An understandable offshoot of this
ideal was the belief that the apparent freedom
from caries enjoyed by so-called primitive races
could be attributed to the “natural” diet on
which they subsisted. Eating hard, fibrous, and

unprocessed food, so the theory went, led to
better development of the jaws and teeth and
helped to clear food debris from the teeth. By
contrast, Europeans were even then eating a lot
of processed food, high in fermentable carbohy-
drates, which was thought to exercise the masti-
catory apparatus insufficiently and lead
eventually to tooth decay. Against the back-
ground of these beliefs, Miller, in the late nine-
teenth century, put forward his chemoparasitic
theory of the development of dental caries.
Miller’s theory, developed during the “golden
age of bacteriology,” was based on the action of
microorganisms on fermentable carbohydrates
that adhered to the tooth’s surface.149 Modern
research shows that Miller’s view of the overall
picture was reasonably correct.
Theories about the preventive value of con-
sumption of hard and fibrous foods became
more widespread in the early twentieth century
and became established dogma in many places.
One such article of faith stated that accumula-
tions of fermentable carbohydrates could be
removed by eating hard and fibrous foods,228
the so-called cleansing or detersive foods.
Another view was that, if a meal were finished
with a salivary stimulant such as an apple,
the mouth would be kept free of fermentation
both by the physical cleansing effect of the
fibrous food and also by the salivary flow
induced by it.169
As noted in the previous section, “protective”
factors in an unrefined diet have proven hard to
identify. High-fiber diets with a good propor-
tion of unprocessed vegetables are today recom-
mended by all health authorities. The low
cariogenicity of these diets, however, is attribut-
able less to the presence of hard and fibrous
foods than to the relative absence of fermentable
carbohydrates.
Some Major Epidemiologic Studies on Diet and
Caries
World War II Studies
Strict food rationing in Japan made sugar virtu-
ally unobtainable during World War II. After the
war, the mean DMF for 10-year-old children in
1950 was considerably below values recorded
in 1940. However, by 1957 DMF values had
returned to just higher than 1940 levels.205
Norway was occupied by German forces for
much of World War II, a 5- to 6-year period dur-
20 Dental Caries 247
ing which strict food rationing was enforced.
Among children 8-14 years of age, average
height and weight were reduced, which indi-
cated nutritional inadequacies. Dental effects
during the occupation included delayed erup-
tion of teeth, which began to be seen 1-2 years
after rationing began and reached a peak after
the war, returning to normal only in the
1950s.208 Caries in the permanent dentition
was drastically reduced, even after allowance
was made for the effects of delayed eruption,
and the number of children ages 7-8 who were
free of detectable caries increased threefold to
fourfold between 1941 and 1946.209 Caries
prevalence returned to 1941 levels by 1949,
after rationing had ended.210 Perhaps the most
fascinating part of these Norwegian studies is
the fact that they were done at all, given the con-
ditions of the occupation.
Tristan da Cunha
The people on the remote island of Tristan da
Cunha in the South Atlantic are mostly of
European descent. The island’s limited contacts
with the outside world were gradually increas-
ing when a volcanic eruption in the early 1960s
led to the temporary evacuation of the entire
community to England. The people returned
when the island was habitable again, after
which the establishment of some industry mod-
ernized the economy and created a demand for
consumer goods. Much of the diet now consists
of processed food. The Tristan da Cunha resi-
dents were given dental examinations on the
island in 1932, 1937, and 1953; in England in
1962; and again on the island in 1966. The
results show that the prevalence of caries in the
first permanent molars of 6- to 19-year-olds was
0% in 1932 and 1937 but was 50% in 1962 and
80% in 1966.66 More recent data will indicate
if Tristan da Cunha has shared in the caries
decline of more recent years.
Hopewood House
The Hopewood House institution in Australia
provided an opportunity for a 15-year study of a
group of children living on a basically vegetar-
ian diet with severely restricted sucrose intake.
The study began with 81 children, ages 4-9
years, of whom 63 (77.8%) had no detectable
caries.122 At age 13, 53% of the children still
had no detectable caries, compared with 0.4%
248 The Distribution of Oral Diseases and Conditions
of the local noninstitutionalized population of
the same age.201 Over the years some of the
dietary restrictions at the institution were
relaxed, but at the conclusion of the study the
caries prevalence among 13-year-olds was still
only 65.3%.80 Although this study used small
numbers and lacked a rigid research design, the
differences between the Hopewood House chil-
dren and the nearby population were so pro-
found that the dental effects of dietary control
were difficult to question.
Anthropologic Studies
There are numerous reports of the disastrously
rapid increase in caries that occurs when an
indigenous society comes in contact with the
diet and lifestyle of high-income nations.
Although the changes in such people’s lives are
often so culturally profound and abrupt that it is
difficult to be sure that all changes in caries
prevalence are due to diet, there is little question
that the dietary factors are important. Examples
of such instances have been reported in
Polynesia,16 Ghana,114 and Greenland,93,153,168
among the Inuit people of Canada’s North-
west,53 among Australian aborigines,185,186 and
among children on a remote Scottish island
where a modern lifestyle replaced traditional
ways.78,79
Hereditary Fructose Intolerance
The rare disease of hereditary fructose intoler-
ance (HFI) requires that people who have it
greatly minimize their sugar intake on a lifelong
basis. Studies of persons with HFI, hard to con-
duct because of the rarity of the condition, show
that they experience virtually no caries com-
pared with normal subjects without HFI.163
Although the numbers of people studied are
necessarily small, the differences in the intake
of sugars and in caries experience are extreme
and obvious.
Vipehölm
The best-known attempt to conduct an experi-
mental study on the effect of diet on dental
decay in humans was the Vipehölm study, car-
ried out in Sweden between 1945 and 1952.75
The study was conducted in a mental institu-
tion, and by today’s standards it would be con-
sidered unethical because it fed high quantities
of sugars to people unable to give their
informed consent to this regimen. Be that as it
may, its conclusions profoundly influenced
the views on the role of sugars in dental decay.
The study design was complicated and not free
of flaws. Briefly, inmates of the institution were
divided into groups with controlled consump-
tion of refined sugars that varied in amount,
frequency, physical form, and time of con-
sumption (with or between meals). The
extremes of intake were (1) no added sugars at
all, and (2) daily between-meal consumption
of 24 sticky toffees, each of which was too large
to be swallowed and so had to be sucked and
chewed. The differences in caries incidence
between the groups were pronounced. Some of
the conclusions of the Vipehölm study can be
challenged in light of more recent research, but
they are listed in Box 20-2 because of the his-
torical importance of this study.
Sugars-Caries Relationships in Today’s
Low-Caries Environment
The major studies described earlier were all
conducted in the prefluoride era when caries
was widespread and severe in high-income
countries. In light of modern research pro-
tocols, design and analysis can be criticized in
virtually all of them: all studies except the
Vipehölm investigation were cross-sectional,
and analysis considered only sugar intake
(measured in various ways) and caries status.
In the period of caries decline, however,
we have to think that the “Vipehölm rules”
have changed. Are all the children with no
BOX 20-2 Summarized Conclusions of the
Vipehölm Study, 1946-5275
●
Sugar consumption increases caries activity.
●
The risk of increased caries activity is greater if the
sugar is in sticky form.
●
The risk is greatest if the sugar is taken between
meals and in a sticky form.
●
The increase in caries under uniform conditions
shows great individual variation.
●
The increase in caries disappears on withdrawal of
sticky foodstuffs from the diet.
●
Caries can still occur in the absence of refined sugar,
natural sugars, and high total dietary carbohydrates.
Reprint by permission of Taylor & Francis AS.

detectable caries we see today not consuming
sugar, or are other factors having a major influ-
ence? Studies such as those suggesting that oral
hygiene is an important covariable in the sug-
ars-caries relationship82,103,203 have raised
questions about the validity of the Vipehölm
findings.
Two prospective studies reported in the
1980s, one in Britain and one in the United
States, measured diet and caries incidence con-
currently and included more analytical detail
than did any previous research. The British
study followed 405 children with an average
initial age of 11.5 years for 2 years.177 The chil-
dren, all from a low-fluoride area near
Newcastle, completed five food diaries, each for
a 3-day period, for a total of 15 days of recorded
diet over the 2 years. Interviews with a dietitian
followed each 3-day period to clarify uncertain-
ties and to quantify amounts. The mean DMFS
incidence of the group was 3.63 over the 2 years,
with 57% of new lesions in pits and fissures, a
lower caries increment than the authors had
expected. Average consumption of all sugars
was 118 g/day, providing 21% of energy intake.
The results showed that caries increment was
weakly but significantly correlated with total
intake of sugars, but poorly correlated with fre-
quency of intake. The authors stated that,
because of the lower than expected caries incre-
ment, more clear-cut results would have been
likely if the study had been extended for
another year.
The second study was based in the low-fluo-
ride area of Coldwater, Michigan. It followed
499 children, initially ages 11-15, for 3 years.38
The majority completed four 24-hour dietary
recall interviews with a dietitian, although 27%
completed more interviews. The boys in the
study averaged 156 g of sugar intake per day
from all sources, the girls 127 g; sugars
accounted for 26% of total energy intake. Both
of these measures are higher than was found in
the British group. Caries incidence was lower
than in the British group, however, averaging
2.9 DMF surfaces over the 3 years, of which 81%
were pit-and-fissure lesions (buccal pits and lin-
gual extensions as well as occlusal lesions).
Nearly 30% of the group developed no caries at
all over the 3 years, and only 51 children
(10.2%) developed two or more proximal
lesions during the study. Only in this latter
20 Dental Caries 249
“high-caries” group was caries experience
related to total intake of sugars, and that rela-
tionship was weak. No relationship was found
between caries experience and frequency of
consumption. The relative risk of caries from
high sugar consumption compared with low
sugar consumption was small42; each addi-
tional 5 g of sugar ingested daily was associated
with a 1% increase in the probability of devel-
oping caries.204
Despite some differences in study protocols,
findings in these two independent studies were
generally similar. Between them, the studies
indicated that consumption of sugars is not a
major risk factor for many children (i.e., those
with no caries despite consumption of a lot of
sugar), but it is for those who are still clearly
susceptible to caries (broadly defined here as
the minority who got proximal-surface caries).
A similar conclusion was reached in a system-
atic review of the caries-sugar relationship in
countries where there is widespread exposure to
fluoride.41
The much-stressed role of frequency of con-
sumption of sugars (“it’s not how much you eat,
it’s how often you eat it”) is clearly called into
question by the studies in Newcastle and
Michigan, as it has been by others in
Sweden.21,198,202 The importance of frequency
of consumption was a major finding of the
Vipehölm study, and it has dominated dental
health education ever since. However, the
importance of frequency in Vipehölm was
based principally on the caries experience of the
group that consumed 24 large toffees between
meals each day, a frequency of consumption
that was not even approached in either the
British or the Michigan study. The results from
the highly artificial circumstances of the
Vipehölm study thus may be misleading when
generalized to the population. (The implica-
tions of these findings for dental health educa-
tion are discussed in Chapter 28.)
Caries and Soft Drinks
As discussed earlier, sugar in liquid form is cari-
ogenic. Sugar in liquid form served well to
induce demineralization in landmark experi-
mental caries studies.226 There is more recent
evidence to show that soft drink consumption is
related to caries: the more soft drinks con-
sumed, the greater the extent and severity of
250 The Distribution of Oral Diseases and Conditions
caries.95,121,138,229 Soft drinks have also been
implicated as part of the cause of the global
epidemic of obesity in children,134 because it is
now common to find soft drinks and juices
replacing formula and milk for children up to
2 years of age.137 Therefore the subject has seri-
ous health implications that go beyond den-
tistry and is yet another example of a public
general health problem that has clear dental
overtones. (This issue is discussed further in
Chapter 28.)
ROOT CARIES
Root caries is defined as caries that begins on
cemental root surfaces below the cervical mar-
gin. It thus is found only where loss of
periodontal attachment has led to exposure of
the roots to the oral environment and hence to
the accumulation of bacterial plaque around
these exposed roots. Root caries appears to be
polymicrobial,189,223 with the bacterial compo-
sition of dental plaque in root lesions appar-
ently little different from that of plaque found
in coronal lesions.32,61,69 As with coronal caries,
sugars are part of the etiology.167
Root caries has been with humankind since
our earliest days; indeed, most of the caries found
in skulls dating from the Stone Age or earlier is
root caries.99,100,154 A similar pattern can be
found today in some low-income coun-
60
Female
50 Male
40
Percent
30
20
10
0
18-24 25-34
Fig. 20-11 Prevalence of root caries in U.S. adults and seniors by gender, 1988-94.213
tries.129,132,187 In high-income countries, general
awareness of root caries only increased in the early
1980s with the realization that older adults were
retaining more teeth than they had previously.
Subsequent studies have confirmed that root
caries is highly prevalent among older persons in
high-income countries.14,18,49,71,84,124,126,157,181
In NHANES III, the prevalence of root caries
among American adults ages 18 or older was
25.1%.232 Prevalence reached over 50% in men
ages 65 or older and in women ages 75 or older.
Prevalence varies in more localized surveys
according to the age and nature of the popula-
tion examined. Localized surveys in parts of the
United States and Canada have found that inci-
dence can range from 0.3 to 0.6 surfaces per per-
son per year.77,118,120
Fig. 20-11 shows the prevalence of root caries
by age among dentate adults in NHANES III.
Males appear to be more affected than females.
Although the condition is more prevalent in
older age-groups, it is not uncommon among
younger people. It is not yet clear whether these
data represent a cohort pattern or whether the
younger age-groups will look like the current
older cohorts in the years ahead. One argument
is that, as more teeth are retained, the number
of surfaces at risk of root caries will increase. But
if gingival recession becomes less common,
then the overall prevalence and severity may not
change much.
35-44 45-54 55-64 65-74 75+
Age-group

Root caries, by definition, is strongly associ-
ated with the loss of periodontal attach-
ment.118,125,173,193,224,231 Other factors found
to be associated with root caries are primarily
socioeconomic, such as years of education,
number of remaining teeth, use of dental serv-
ices, oral hygiene levels, and preventive behav-
ior.18,54,86,225 An important risk factor is also
the use of multiple medications among the eld-
erly,102 a common practice in nursing homes
and one that can promote xerostomia (salivary
diminution). Xerostomia has long been known
as a major risk factor for caries among people
of any age and is particularly prevalent among
those who have received radiation treatment
for cancer.8 Other risk factors identified in a
representative British sample of people ages 65
or older were practicing poor oral hygiene,
wearing partial dentures, sucking candies in a
dry mouth, and living in an institution.199
People who suffer from coronal caries also
seem likely to be at risk of root caries when gin-
gival recession occurs,19,225 and root caries is
less prevalent in high-fluoride areas than it is in
6
White
African-American
5
Mexican-American
Mean root lesions per person
0
18-24 25-34
Fig. 20-12 Mean number of root lesions in whites, African-Americans, and Mexican-American by age in the United
States, 1988-94.213
20 Dental Caries 251
low-fluoride communities.40,197 Smokers
exhibit more root caries than nonsmokers, and
severity tends to be inversely related to the
number of teeth remaining.18,125
With regard to racial distribution, Fig. 20-12
shows the average number of root lesions in
whites, African-Americans and Mexican-
Americans as found in NHANES III. This graph
suggests that African-Americans of most ages
average more root lesions per person than do
the other groups.
Root caries seems to be a particular problem
among older people of lower SES, those who
have lost some teeth, those who do not main-
tain good oral hygiene, and those who do not
visit the dentist regularly. Because of the aging
of the population and increasing retention of
teeth, the dimensions of the root caries problem
are likely to continue to grow in the future, even
if the number of lesions per person shows little
change. The attention of dental practitioners
should be increasingly devoted to treating and
preventing root caries in adults, as less time is
needed to deal with coronal caries in children.
35-44 45-54 55-64 65-74 75+
Age-group
252 The Distribution of Oral Diseases and Conditions
EARLY CHILDHOOD CARIES
Early childhood caries (ECC) is a distressing syn-
drome characterized by severe caries in the pri-
mary maxillary incisors of infants, typically
those 1-3 years old. Total destruction of tooth
crowns is common, other teeth in the mouth are
usually involved, and ECC is difficult and expen-
sive to treat.227 There has long been confusion
over the name of the condition,91 which has var-
iously been called nursing caries, labial caries, and
baby bottle tooth decay, among other things,
because the condition was seen to arise from
prolonged infant feeding by either bottle or
breast. Now it is understood that broader expo-
sure to cariogenic diets can also be a factor.55,212
The role of prolonged feeding with milk, either
human or cow’s, to which no further sugar has
been added is uncertain. A systematic review of
breastfeeding as a risk factor for ECC could reach
no conclusions because the literature was
marked by inconsistent study methods and case
definitions.222 Milk does not promote caries in
laboratory studies,28 and another systematic
review concluded that the evidence for even pro-
longed use of the bottle as a risk factor in ECC is
weak.172 Prolonged exposure to liquids with
added sugars or to high-sugar fluids such as soft
drinks or fruit juices is considered the main cul-
prit, but, again, precise evidence is elusive.
In the United States prevalence of ECC at the
national level is extremely low, but in particular
groups in which ECC is concentrated, preva-
lence can be as high as 70%.150 A cursory visual
inspection of children ages 12-23 months in
NHANES III found a 2% prevalence, with most
cases among children of Mexican-American her-
itage.96 ECC is prevalent among immigrants to
the United States and among Native
Americans,31,230 as well as among indigenous
peoples elsewhere.4,6 It is more prevalent in
lower SES populations and among infants who
are being cared for by persons with little educa-
tion.150 ECC has been associated with lower
than average growth among affected infants,11
and children with the condition seem to be at
greater risk for caries in the permanent denti-
tion later in life.97 These latter observations may
reflect chronically poor and cariogenic diets
rather than direct cause and effect.
Research into the condition has been ham-
pered by absence of a clear case definition.
Caries of the primary maxillary incisors, often
with little if any caries of primary molars, is the
most common case definition, but some inves-
tigators have defined it as generalized rampant
caries or the presence of caries on the buccal
and lingual surfaces of the incisors. In an effort
to reach a clear case definition, a workshop
group in 1999 took the view that any caries
before 6 years of age is ECC and that there are
degrees of severity above that, referred to as
severe early childhood caries, or S-ECC (see
Chapter 15). Whether this approach to the
problem will clarify the issue remains to be
seen.
Prevention of ECC has been based largely on
education, but it is clear that simply pointing out
to parents the dangers of excessive feeding with
sugary liquids is by itself ineffective.230 A better
understanding of the social and cultural factors
involved among the population groups most
affected is clearly needed if the prevalence of ECC
is to be seriously reduced among affected groups.
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 21 Periodontal Diseases
PERIODONTAL INFECTIONS AND HOST
RESPONSE
CURRENT MODELS OF PERIODONTAL
DISEASES
DISTRIBUTION OF PERIODONTAL DISEASES
Geographic Distribution
Prevalence of Gingivitis
Prevalence of Periodontitis
Incidence of Periodontitis
DEMOGRAPHIC RISK FACTORS IN
PERIODONTITIS
Gender and Race or Ethnicity
Age
Socioeconomic Status
Genetics
The term periodontal disease has long been recog-
nized as a generic term used to describe a group
of diseases, so it should more correctly be used
in the plural form. It is generally more useful to
refer specifically to gingivitis and periodontitis,
with the term periodontal diseases reserved only
for those situations in which the generic term is
specifically intended.
This chapter describes the epidemiology of
gingivitis and adult periodontitis, their distribu-
tion, and the risk factors and background char-
acteristics associated with them. Periodontal
diseases have been prevalent throughout human
history, although without the obvious secular
variations that characterize dental caries.
Human remains from the early Christian era
show clear evidence of periodontal bone loss.156
PERIODONTAL INFECTIONS
AND HOST RESPONSE
Both gingivitis and periodontitis result from
bacterial infections. The expression of clinical
disease, however, is a function of both bacterial
RISK FACTORS FOR PERIODONTITIS
Oral Hygiene, Plaque, and Microbiota
Local Factors
Nutrition
Tobacco Use
Psychosocial Stress
PERIODONTITIS AND SYSTEMIC
CONDITIONS
Diabetes
HIV Infection
Cardiovascular Disorders
Osteoporosis
Adverse Pregnancy Outcomes
PREDICTION OF PERIODONTITIS
infection and the host response to that infec-
tion, mediated by environmental factors like
smoking and oral hygiene. Gingivitis is an
inflammatory process of the gingiva in which
the junctional epithelium, although altered by
the disease, remains attached to the tooth at its
original level. There are initial, early, and estab-
lished gingivitis lesions, and a sequential micro-
bial colonization leads to bacteriologically
more complex plaque as the lesions progress.176
Periodontitis is also an inflammatory condi-
tion of the gingival tissues, characterized by
clinical attachment loss (CAL) of the periodon-
tal ligament and loss of bony support of the
tooth. Periodontitis develops as an extension of
gingivitis, although only a small proportion of
gingivitis sites make this transition.112,124,139
What happens in this transition is that
supragingival plaque serves as a reservoir for
periodontopathogenic organisms,71,201,251 and
when this infection is strong enough to over-
whelm the host defense, bacteria in supragingi-
val plaque migrate subgingivally to form a
subgingival biofilm.180 Inflammatory media-
259
260 The Distribution of Oral Diseases and Conditions
tors play an important role in the progression of
periodontitis.166,177 A number of microbial
species have been associated with destructive
periodontitis, although it is unlikely that all of
these bacteria are essential players in the dis-
ease.179 As is discussed later in this chapter,
some of these species have been associated with
serious systemic diseases.
Whether or not periodontitis develops after
infection, and its severity if it does, are deter-
mined by the nature and extent of the host
response to these infections. Only some 20% of
periodontal diseases are now attributed to bac-
terial variance, 50% are attributed to genetic
variance, and 20% to tobacco use,180 although
the contribution of tobacco use may be higher
than that.93 Only a small proportion of virtu-
ally any population is susceptible to severe,
generalized periodontitis, even though most
people have these infections to some degree.
This has led to the hypothesis that there are two
distinct types of periodontitis. One is the plaque
and local factors type, the most common form,
in which specific pathogens dominate the host
response in controlling disease expression; the
second is the compromised host type, in which
severity and rate of progression are often rapid
and are not well correlated with local factors
like plaque deposits.166 The compromised host
type is less common, responds much less favor-
ably to standard treatments, and is thought to
be the type of disease found in aggressive and
diabetes-associated periodontitis. Neutrophil
abnormalities have been associated with the
compromised host form of the disease,178 and
at least in aggressive periodontitis the compro-
mised host response is thought to be of genetic
origin.50
Many different classifications of periodon-
tal diseases have been proposed; their evolu-
tion is well documented in the various world
workshops held down the years. These work-
shops are international gatherings of experts to
review the state of knowledge in the periodon-
tal field and were held in 1966, 191 1977, 110
1989,163 and 1996 (reported in the first issue
of Annals of Periodontology). A subsequent
workshop in 1999, held to review disease classi-
fications, produced the list shown in Box 21-1.
This classification is far more detailed than its
predecessor. 163 It is becoming increasingly
accepted that the periodontal diseases are a
family of more or less related conditions, and
advances in molecular biology will most likely
provide new bases for classifying them in the
future.
Although these different categories of peri-
odontitis are widely recognized, there are no
generally accepted definitions of serious or mod-
erate periodontitis, terms widely used in clinical
practice, epidemiology, and public health.
Several definitions of serious periodontitis that
have been used in epidemiologic studies are
shown in Box 21-2. Two of these definitions use
CAL plus the presence of pockets, whereas the
third is based on a cutpoint on a statistical dis-
tribution. When the term serious or severe peri-
odontitis is used in this chapter, the reference is
to a degree of periodontitis severe enough to
cause or threaten the loss of teeth. There is mod-
erate agreement in the literature that CAL of
6 mm or more is a reasonable cutoff point to
differentiate serious from moderate periodonti-
tis; the latter term is usually applied to CAL of
4-5 mm or less. Moderate periodontitis is used in
this chapter to mean periodontitis in which
pocketing, CAL, or even some bone loss can be
clinically or radiographically demonstrated, but
the condition is not yet severe enough to
threaten the loss of teeth.
CURRENT MODELS OF PERIODONTAL
DISEASES
As mentioned in Chapter 16, perceptions of
the nature of periodontal diseases changed
radically as a result of research during the
1980s and 1990s. The old view of periodontal
disease before that time is summarized in the
following statement from a 1961 report by an
expert committee of the World Health
Organization (WHO):
Periodontal disease is one of the most widespread dis-
eases of mankind. No nation and no area of the world is
free from it and in most it has a high prevalence, affecting
in some degree approximately half the child population
and almost the entire adult population. Research and clin-
ical evidence indicate that the damage caused to the sup-
porting structures of the teeth by periodontal disease in
early adult life is irreparable, while in the middle adult life
it destroys a large part of the natural dentition and
deprives many people of all their teeth long before old age.
The total effect of periodontal disease on the general
health of the populations is unassessable.250

BOX 21-1 Summarized Classification of Gingival and Periodontal Conditions11
Gingival Diseases
Dental plaque–induced gingival diseases
Gingivitis associated with dental plaque only
Gingival diseases modified by systemic factors
Gingival diseases modified by medications
Gingival diseases modified by malnutrition
Non–plaque-induced gingival lesions
Gingival diseases of specific bacterial origin
Gingival diseases of viral origin
Gingival diseases of fungal origin
Gingival diseases of genetic origin
Gingival manifestations of systemic conditions
Traumatic lesions
Foreign body reactions
Not otherwise specified
Chronic Periodontitis
Localized
Generalized
Aggressive Periodontitis
Localized
Generalized
Periodontitis As a Manifestation of Systemic Diseases
Associated with hematologic disorders
Associated with genetic disorders
Not otherwise specified
BOX 21-2 Some Definitions of “Serious”
Periodontitis Used in Periodontal Studies
●
Four or more sites with loss of periodontal
attachment (CAL) of ≥5 mm, with pocket depth of
≥4 mm at one or more of those sites26
●
Two or more teeth with CAL of ≥6 mm, plus one or
more sites with pocket depth of ≥5 mm137
●
Mean CAL in the top 20th percentile of the
distribution129
This whole passage conjures up a vision of
helpless peoples, all equally susceptible and
suffering en masse. It was also accepted at that
time that gingivitis invariably progressed to
periodontitis, a view that has now changed to
21 Periodontal Diseases 261
Necrotizing Periodontal Diseases
Necrotizing ulcerative gingivitis
Necrotizing ulcerative periodontitis
Abscesses of the Periodontium
Gingival abscess
Periodontal abscess
Pericoronal abscess
Periodontitis Associated With Endodontic Lesions
Combined periodontic-endodontic lesions
Developmental or Acquired Deformities
and Conditions
Localized tooth-related factors that modify or
predispose to plaque-induced gingival
diseases/periodontitis
Mucogingival deformities and conditions around
teeth
Mucogingival deformities and conditions on
edentulous ridges
Occlusal trauma
recognition that few gingivitis lesions actually
make that transition.
Challenges to the concept of universal sus-
ceptibility came with epidemiologic studies in
low-income countries. These surveys yielded
broadly similar results in that they found mas-
sive deposits of plaque and calculus, and thus
high levels of gingivitis.21 But contrary to expec-
tations, they also found that the prevalence of
serious, generalized periodontitis in these
poorer countries was little different from that in
the highly treated populations of high-income
countries.16,17,19,122,131,170 Further substantial
modification to the traditional perception of
periodontitis came with the demonstration in
the early 1980s that the periodontal tissues
apparently had the capacity to repair them-
selves.75 This finding was incorporated into
262 The Distribution of Oral Diseases and Conditions
what became known as the burst theory of peri-
odontitis,211 which essentially states that
periodontitis progresses in a series of relatively
short, acute bursts of rapid tissue destruction,
followed by some tissue repair and long periods
of remission.125 This view was the converse of
the hypothesis of linear progression that had
been assumed until that time and resulted from
analyzing measurements from individual sites
rather than using pooled data as had been done
before. The burst theory of periodontal destruc-
tion has been accepted by most researchers, and
there is now good epidemiologic evidence to
support it.28
Basic, clinical, and epidemiologic research
from around the late 1970s onward (about the
same time that the caries decline was recog-
nized) has therefore led to a perception of the
periodontal diseases that can be summarized as
shown in Box 21-3.
Although periodontal diseases are constantly
becoming better understood, the measurement
problems described in Chapter 16 have not
gone away. We are still not confident about how
to separate susceptible from nonsusceptible
people and active from inactive sites.174 Until
research finds a suitable way of measuring
active disease, then CAL, pocket depth, radi-
ographic bone loss, and gingival bleeding must
serve as measures of periodontal diseases, cum-
bersome and inappropriate for some purposes
though they are.
DISTRIBUTION OF PERIODONTAL
DISEASES
Geographic Distribution
Over 70% of adults in all parts of the world
have some degree of gingivitis or
periodontitis.20 Under the old perception of
periodontal disease, it was considered that
prevalence and severity were greater in low-
income countries than in the higher-income
world. However, data collected since 1980 in
WHO’s Global Oral Health Data Bank,187,188
when added to the results of other epidemio-
logic studies,15 suggest that, although gingivitis
and calculus deposits are more prevalent and
severe in low-income nations, there are fewer
global differences in the prevalence of severe
periodontitis. Gingivitis and calculus deposits
can be controlled by personal oral hygiene and
BOX 21-3 A Current Model of Periodontal
Diseases
●
Only a small proportion of persons (5%-15%)
exhibit severe periodontitis, where “severe” means
that tooth loss occurs or is threatened. Mild
gingivitis is common, as is mild to moderate
periodontitis. Most adults exhibit some loss of bony
support and loss of probing attachment while still
maintaining a functioning dentition.
●
Gingivitis and periodontitis are associated with
bacterial flora that have some similarities but also
some differences between the two conditions.
Gingivitis precedes periodontitis, but only a fraction
of sites with gingivitis later develop periodontitis.
●
Although periodontitis is usually related to age in
cross-sectional surveys, it is not a natural
consequence of aging.
●
Periodontitis is not the major cause of tooth loss in
adults, except perhaps in the oldest age-groups in
some populations.
●
Periodontitis is usually a site-specific condition and
is only occasionally seen in generalized forms.
Generalized periodontitis is usually severe and of the
early-onset type.
●
Periodontitis is usually thought to proceed in bursts
of destructive activity with quiescent periods
between the bursts.
professional dental care, so it is to be expected
that they are less severe in high-income
nations. This geographic profile, in which
severe periodontitis is not clearly dependent on
the presence of plaque and calculus, is consis-
tent with the compromised host model of peri-
odontitis described earlier.
Prevalence of Gingivitis
At the population level, gingivitis is found in
early childhood, is more prevalent and severe
in adolescence, and tends to level off after that.
The prevalence of gingivitis among school-
children in the United States has been around
40%-60% in various national surveys.235 In a
national survey of employed adults in 1985-
86, 47% of males and 39% of females ages 18-
64 had at least one site that bled on
probing.237 In the first national survey of
adults that measured gingivitis, conducted in
1960-62, some 85% of men and 79% of

women were affected.234 Even with allowance
for the differences between the two surveys in
measurement techniques and the populations
studied, it seems fairly clear that there has been
an improvement in gingival health over that
period.171
Gingivitis is closely correlated with plaque
deposits, a relationship long considered one of
cause and effect. Studies of the natural history of
periodontal diseases in Norway and Sri Lanka
found no increase in prevalence and severity of
gingivitis between the late teen years and age 40.
In Norwegian professionals and students,
among whom oral hygiene was excellent,8 and
in Sri Lankan tea workers, among whom gingi-
val conditions and oral hygiene were poorer,
there was no age-related increase in gingivitis.
Surveys in other low-income countries show
that gingivitis, associated with extensive plaque
and calculus deposits, is the norm among
adults.15
Gingivitis is likely to have declined over
recent years in the United States because of
greater attention to oral hygiene as a part of per-
sonal grooming. The main research interest in
gingivitis today is why some lesions progress to
periodontitis and some do not, and what fac-
tors may predict these outcomes.
Prevalence of Periodontitis
Interpretation of epidemiologic data from
before 1980 or so is difficult because the
indexes used to measure the conditions before
that time are no longer considered valid
(see Chapter 16). The impression created by
these data was that summed up in the WHO
quotation given earlier: “periodontal disease”
was uniformly extensive and serious in most
populations. Later research, however, in which
the use of disaggregated indexes in epidemiol-
ogy played a prominent part, has led to an
almost total reversal of that concept. Data from
many parts of the world have now shown that
the prevalence of generalized, severe periodon-
titis is in the range of 5%-15% in almost all
populations, regardless of their state of eco-
nomic development, conditions of oral
hygiene, or availability of dental care.15,51,112,229
This relatively low proportion supports a funda-
mental shift away from the old view of universal
susceptibility, even though it still represents a
lot of people with serious periodontitis.
21 Periodontal Diseases 263
Any assessment of the prevalence of a con-
dition, and the form of its distribution in a
population, must begin with a case definition
of the disease. Here is the first difficulty, for as
described earlier there is no clear agreement
on how to define moderate and serious peri-
odontitis. We stated earlier that 6-mm CAL is
generally considered serious and 4- to 5-mm
CAL moderate, but to many it seems reason-
able to say that any CAL should be considered
disease. Philosophically that may be true, but
in practical terms considering all CAL as dis-
ease is not helpful. To illustrate this point,
Fig. 21-1 graphs the proportion of adults in
the United States with at least one site show-
ing 2-mm CAL. A high proportion of even the
younger age-groups is affected, and the condi-
tion soon becomes almost universal. CAL of at
least 2 mm is so common, and is so often
found in persons with functional dentitions,
that one has to wonder whether philosophi-
cally it should be thought of as disease in a
clinical sense. Certainly any criterion that is so
commonly met is not useful in epidemiologic
research in which risk factors are being
sought.
CAL is considered to be the most valid
measure of periodontitis, 74 even though it
measures past disease rather than present
activity. If CAL of 2 mm is too common to
discriminate between people who are suscep-
tible and those who are not susceptible to seri-
ous periodontitis, then where should the
cutoff be? Fig. 21-2 graphs the proportion of
adults with at least one site showing CAL of
2 mm, 4 mm, or 6 mm, and Fig. 21-3 shows
the skewed distribution of CAL in three age-
groups. If the use of a 2-mm measure is not
sensitive enough (i.e., includes too many false
negatives), a 6-mm cutoff may be not specific
enough (i.e., it could exclude too many true
positives). We stated earlier that CAL of 4-5
mm has generally been considered moderate
periodontitis in the literature, so CAL of at
least 3 mm, at the upper end of mild peri-
odontitis, seems a reasonable basis for a case
definition of periodontitis. In incidence stud-
ies, 3-mm CAL is usually taken as the criterion
for incident periodontitis because this level is
outside the change that could reasonably be
attributed to error by a trained, experienced
examiner.25
264 The Distribution of Oral Diseases and Conditions

100
Female
Male
80

Percent 60

40

20

0
18-24 25-34 35-44 45-54 55-64 65-74 75+

Age-group

Fig. 21-1 Proportion of U.S. adults with at least one site showing clinical attachment loss of 2 mm or more by age
and gender, 1985-86.233

Carolina, so named for the five-county geo-

Incidence of Periodontitis
Longitudinal studies of periodontitis onset and
progression in community-dwelling popula-
tions are inherently expensive and difficult, so it
is not surprising that only a few have been con-
ducted. One was the Piedmont project in North
graphic region in which a community-dwelling
sample (i.e., neither institutionalized nor taken
from patient lists at a dental school) ages 65-80
years, mostly rural and of low income, received a
series of periodontal examinations in their own
homes over 5 years. Periodontal conditions in

100
2 mm or more
4 mm or more
80
6 mm or more

60
Percent

40

20

0
18-24 25-34 35-44 45-54 55-64 65-74 75+

Age-group

Fig. 21-2 Proportion of U.S. adults with at least one site showing clinical attachment loss of 2 mm or more, 4 mm
or more, and 6 mm or more, by age, 1988-94.233

100
80
Cumulative percent
60
40
20
0
2 3 4 5
Loss of periodontal attachment (mm)
Fig. 21-3 Cumulative proportion of U.S. adults ages 18-44, 45-64, and 65 or older showing varying degrees of
clinical attachment loss at most severely affected site, 1988-94.233
this group were generally not good. Although
the mean number of affected sites at baseline
was only a little more than that found in
younger age-groups, the severity of disease at
those sites was considerably greater.26 When dis-
ease incidence (defined as an increase in CAL of
at least 3 mm) was assessed for the first 18
months and for the second 18 months sepa-
rately, CAL during the first period was positively
related to CAL in the second period at the level
of the individual but not at the site level.24 These
findings were confirmed at the 5-year examina-
tion: the presence of CAL in the first period did
not put a site at risk for CAL in subsequent peri-
ods.27 These findings support the episodic, ran-
domized model of periodontitis in susceptible
persons. At the mesiobuccal sites examined,
increased pocket depth rather than gingival
recession accounted for most disease incidence,
whereas for buccal sites gingival recession
accounted for most incidence.23 The research
team found that risk factors were not the same as
prognostic factors (their term for risk factors
related to the progression of existing disease).
However, counted among both risk and prog-
nostic factors were low income, tobacco use,
presence of specific bacteria, and use of medica-
tions likely to result in soft tissue reactions.
21 Periodontal Diseases 265
18-44
45-64
65+
6 7 8 9 10 11 12+
A longitudinal project of major importance
was the 15-year study of periodontitis among
480 tea workers in Sri Lanka.131 The group stud-
ied had virtually no dental treatment of the type
found in developed countries, so the data
reflected the natural history of periodontitis.
Based on tooth loss and interproximal CAL over
the 15 years of the study, it was concluded that
some 8% demonstrated rapid progression, 81%
moderate progression, and 11% no progression
beyond gingivitis. This study provided impor-
tant evidence demonstrating the range of sus-
ceptibility to periodontitis. A subsequent
finding on disease incidence in this group was
that gingival recession progressed over time on
virtually all surfaces, whereas in a comparison
group of high-income Norwegians it was largely
confined to the buccal surfaces. The buccal-only
recession was thought to come from toothbrush
abrasion, whereas the all-surfaces recession
among the Sri Lankans was seen as plaque
related.130
Clinical studies that have followed groups of
patients over a period of time have contributed
valuable information toward the understanding
of periodontitis.73,84,127 These should not be
called epidemiologic studies, for when patients
are followed then all participants, by definition,
266 The Distribution of Oral Diseases and Conditions
are susceptible to the disease. Although epi-
demiologic research is better for defining risk
factors, clinical studies are valuable for studying
disease progression in susceptible individuals.
DEMOGRAPHIC RISK FACTORS
IN PERIODONTITIS
Gender and Race or Ethnicity
Surveys of periodontal conditions usually show
that men have poorer periodontal health than
women. This has long been observed and is still
the case in the most recent national survey in
the United States. Figs. 21-1, 21-4, and 21-5
show that, as measured by CAL, the presence of
pockets, and subgingival calculus, women con-
sistently look better than men. In older sur-
veys234,236 this finding was obscured by the
greater tooth loss among women, tooth loss
that was assumed to reflect the ravages of peri-
odontal disease. More recently, however, differ-
ences in tooth loss between the sexes are no
longer evident (see Chapter 19). Women usu-
ally exhibit better oral hygiene than do men,237
which would explain the differences seen in
gingivitis. The fact that women show less sub-
gingival calculus (see Fig. 21-5) is likely to con-
35
Female
30 Male
25
20
Percent
15
10
0
18-24 25-34
Fig. 21-4 Proportion of U.S. adults with at least one periodontal pocket of 4 mm or more by age and gender,
1988-94.233
tribute toward their better periodontal condi-
tions as measured by CAL and pocket depth.
Current knowledge of the pathogenesis of peri-
odontitis, when added to the epidemiologic
evidence, indicates that there are no inherent
differences between men and women in suscep-
tibility to periodontitis.
There is also little evidence to suggest differ-
ent susceptibility to periodontitis among differ-
ent races. Early epidemiologic studies showed
considerable differences between nations190,198
but no consistent associations with race or eth-
nicity when persons of the same age and oral
hygiene status were compared. Reviews pre-
sented at world workshops in 1966243 and
197744 also found no differences in disease
prevalence that could be attributed to race or
ethnicity, and that view essentially still
prevails.15 On the other hand, in the 1986-87
national survey of schoolchildren, the preva-
lence of CAL (at least one site with attachment
loss of 3+ mm) in 13- to 17-year-olds was
10% among African-Americans, 5% among
Hispanics, and only 1.3% among whites.3
These data did not account for socioeconomic
differences, so the differences seen may not be
attributable to race or ethnicity.
35-44 45-54 55-64 65-74 75+
Age-group
 21 Periodontal Diseases 267

80
Female
Male
60

Percent

40

20

0
18-24 25-34 35-44 45-54 55-64 65-74 75+

Age-group

Fig. 21-5 Proportion of U.S. adults with at least one site showing subgingival calculus by age and gender,
1988-94.233

40
Low SES
Middle
30 High SES
Percent

20

10

0
18-24 25-34 35-44 45-54 55-64 65-74 75+

Age-group

Fig. 21-6 Proportion of U.S. adults with at least one site showing clinical attachment loss of 6 mm or more by age
and socioeconomic status (SES), 1988-94.233

Fig. 21-6 shows the extent of severe CAL in the
United States by socioeconomic status (SES),
and Fig. 21-7 shows the prevalence of severe
periodontitis among four racial-ethnic groups in
the United States in the third National Health
and Nutrition Examination Survey (NHANES
III) of 1988-94. Data in these charts are not con-
sistent from one age-group to another except
that prevalence is higher at all ages among
African-Americans, and this pattern is likely to
be associated with SES rather than to reflect
true racial differences. The WHO Global Oral
Health Data Bank, which maintains data from
many nations collected using the Community
268 The Distribution of Oral Diseases and Conditions
60
African-American
Mexican-American
50
White
Other
40
Percent
30
20
10
0
18-24 25-34
Fig. 21-7 Proportion of U.S. adults with at least one site showing clinical attachment loss of 6 mm or more by age
and race or ethnicity, 1988-94.233
Periodontal Index, suggests a rather remark-
able uniformity of conditions around the
world.187,188 Overall, the evidence indicates that
race and ethnicity in themselves cannot be con-
sidered as demographic risk factors for peri-
odontitis.
Age
The relationship between age and periodontitis
is not always an easy one to understand. Much
of the problem dates back to the older percep-
tion of the disease, in which the interpretation
of cross-sectional survey data was generally that
the severity of the disease increased with
advancing age. However, today we do not view
periodontitis as a disease of aging. The greater
prevalence and severity of CAL in older people
in cross-sectional surveys come not from a
greater susceptibility in older people but from
the cumulative progression of lesions over
time.35
Fig. 21-2 shows the distribution of degree of
CAL at the most affected site among adults as
measured by NHANES III in United States dur-
ing 1988-94. These cross-sectional data show
that there is a linear relationship between
35-44 45-54 55-64 65-74 75+
Age-group
age and the proportion of people with at least
one site with 4-mm or 6-mm CAL. By contrast,
the proportion of people with at least one
site with 2-mm CAL rises rapidly with age and
then tends to flatten out at a high level. This
suggests that people who get only this low level
of periodontitis get it early in life, and as dis-
cussed previously it is too common to be
of value in discriminating between disease
and nondisease.
Fig. 21-4 shows that the relationship between
age and the presence of at least one pocket of
4 mm or more is not as direct as that found with
CAL. If pockets are taken to reflect active disease
(as opposed to CAL, which is a “scar” of past
disease), then this weak relationship with age is
not surprising.
Age-related findings were a feature of the Sri
Lankan studies described previously.131 Earlier
reports of these researchers compared the Sri
Lankans with a group of college students and
professors in Oslo, Norway, a dentally conscious
group.8,132,133 The oral hygiene status of the
Oslo group was excellent, with no increase in
the prevalence and severity of gingivitis from the
late teenage years to around 40 years of age.

Mean annual CAL in the Oslo group was 0.07-
0.13 mm. The Sri Lankan group was followed
for 15 years, and as described earlier participants
could be categorized into three groups in terms
of rate of disease progression: rapid, moderate,
and little to none. In the first two groups, peri-
odontitis progressed with age, although natu-
rally much more so in the rapid-progression
group, virtually all of whom were edentulous by
40-45 years of age. In the moderate-progression
group, the annual mean rate of CAL increased
from 0.3 mm when the members were in their
twenties to 0.5 mm 15 years later. By contrast,
annual CAL in the rapid-progression group aver-
aged 1.04 mm when they were ages 25-29. In the
nonprogressing group, average annual CAL was
around 0.05 mm and did not change with age.
Rather than showing an increased susceptibil-
ity to periodontitis with increasing age, post-1980
epidemiologic studies support the view that those
who retain their teeth into old age are likely to be
the less susceptible individuals. When periodon-
titis occurs in susceptible persons, it starts young.*
None of these studies demonstrating moderate
CAL in young people followed their subjects into
later life. These young people may fit the compro-
mised host disease model,166 although without
case-control studies or additional longitudinal
data this cannot be stated for sure. It fits the pat-
tern of many diseases, however, if the persons
most susceptible to periodontitis are those who
exhibit the disease in their youth. (We should
note that we are not referring here to the specific
condition of aggressive periodontitis, which is
thought to affect some 0.1%-0.2% of the adoles-
cent population.)239
The likelihood that older dentate people may
be of low susceptibility is strengthened by the
finding that serious disease is not as common
among such groups as once thought. As shown
in Fig. 21-3, the distribution of people by their
most severe CAL site is skewed, and this skewed
distribution is largely independent of age.91
Other analyses of cross-sectional national sur-
vey data have also concluded that age is not a
major determinant of periodontitis.1,36
Even though there are indications from clini-
cal studies that the aging periodontium does
not tolerate plaque as well as it used to, that the
*References 4,9,16,17,19,38,48,49,88,91,120,131,141,224,
227,249.
21 Periodontal Diseases 269
nature of the plaque itself may change with age,
and that the periodontium recovers from injury
more slowly, these potential problems are over-
shadowed by the patient’s susceptibility to dis-
ease.238 This further supports the idea that,
when a patient is susceptible to periodontitis,
the tendency is seen early. Adult periodontitis in
the elderly is characterized by infrequent and
slow progression, and does not usually lead to
tooth loss. Even in cases in which periodontitis
is reported as a leading cause of tooth loss in the
elderly (see Chapter 19), it is likely that a lot of
the teeth extracted then have been seriously dis-
eased for years rather than becoming that way
in old age.
To summarize the data on age and periodon-
titis: cross-sectional survey data invariably
show, on average, a greater extent of CAL among
older than among younger persons. The appar-
ent increase of CAL with age is more a lifetime
accumulation of effects than a greater suscepti-
bility in the older years. Limited longitudinal
data suggest that CAL increases rapidly with age
among the 5%-15% of any population that is
susceptible to serious disease and to a lesser
extent among the majority that exhibits moder-
ate disease. Those susceptible to serious disease
exhibit CAL and bone loss when young, often in
the teenage years.
Socioeconomic Status
Generally, those who are better educated,
wealthier, and live in better circumstances enjoy
better health status than the less educated and
poorer segments of society. Many disease condi-
tions are associated with SES, a complex vari-
able that can subsume a lot of cultural factors.
Periodontal diseases are among this group13,225
and have historically been related to lower
SES.234,236 The periodontal ill effects of living in
deprived circumstances can start early in life.206
Gingivitis and poorer oral hygiene are clearly
related to lower SES, but the relationship
between periodontitis and SES is less direct.
Fig. 21-8 shows that there are obvious SES differ-
ences only among younger people when CAL is 2
mm or more, but as we have stated several times
already, CAL of 2 mm is not a sensitive measure.
When those with CAL of at least 6 mm (see Fig.
21-6) are classified by SES, a more consistent dif-
ference is seen, especially at younger ages. As
shown in Fig. 21-9, when the measure is the
270 The Distribution of Oral Diseases and Conditions

100
Low SES
Middle
80
High SES

60
Percent

40

20

0
18-24 25-34 35-44 45-54 55-64 65-74 75+

Age-group

Fig. 21-8 Proportion of U.S. adults with at least one site showing clinical attachment loss of 2 mm or more by age
and socioeconomic status (SES), 1988-94.233

50
Low SES
Middle
40
High SES

30
Percent

20

10

0
18-24 25-34 35-44 45-54 55-64 65-74 75+

Age-group

Fig. 21-9 Proportion of U.S. adults with at least one periodontal pocket of 4 mm or more by age and socioeco-
nomic status (SES), 1988-94.233

prevalence of pockets of at least 4 mm, differ-
ences are also seen between SES strata and are
most pronounced among the young. Subgingival
calculus deposits are also more prevalent among
lower SES groups (Fig. 21-10).
The widely observed association between
SES levels and gingival health is a function of
better oral hygiene among the more educated
and a greater frequency of dental visits among
the more dentally aware and those with dental
insurance (who are more likely to be white-col-
lar employees, i.e., those with more education).
SES is a complex and multifaceted variable, and
it is virtually impossible to remove the effect of
SES as a confounder in the race-ethnicity associ-
ations seen in Fig. 21-7.
Genetics
The first report identifying a genetic component
in periodontitis appeared in 1997.113 Most of
the research studies relating to genetics as a
determinant of disease have been laboratory
and clinical investigations rather than epidemi-
ologic studies but they should still be briefly
considered here.
The original 1997 report, based on data from
patients in private practices, found that a
100
Low SES
Middle
80
High SES
60
Percent
40
20
0
18-24 25-34
Fig. 21-10 Proportion of U.S. adults with at least one site showing subgingival calculus by age and socioeconomic
status (SES), 1988-94.233
21 Periodontal Diseases 271
specific genotype of the polymorphic inter-
leukin-1 (IL-1) gene cluster was associated with
more severe periodontitis. This relationship
could only be demonstrated in nonsmokers,
which indicated immediately that the genetic
factor was not as strong a risk factor as was smok-
ing. The IL-1 gene cluster has received a lot of
research attention since then. This is appropriate,
given that the proinflammatory cytokine IL-1 is a
key regulator of the host response to microbial
infection,147 although IL-1 is unlikely to be the
only genetic factor involved.142 IL-1 has been
identified as a contributory cause of periodonti-
tis among some patient groups53,61,116,119 and in
an epidemiologic study.224
Although there is little doubt that periodon-
titis has a genetic component, the strength of
that component is still to be determined. On
the one hand, a study of 169 twin pairs con-
cluded that about half of the variance in peri-
odontitis was attributable to heredity.153 On
the other hand, there were no differences in
tooth loss attributable to IL-1 variation over 10
years in a nonsmoking population with good
periodontic maintenance treatment.39 A com-
bination of IL-1 genotyping and smoking his-
tory may provide a good risk profile for
35-44 45-54 55-64 65-74 75+
Age-group
272 The Distribution of Oral Diseases and Conditions
patients,147 and an interaction between smok-
ing and genetics may be a contributory factor in
severity of periodontitis.150,183 IL-1 has been
described as playing a clear, but not essential,
role in regulating host response to infec-
tion.53,61 Further research, including epidemio-
logic studies of people with and without
disease, are necessary before the genetic contri-
bution to the initiation and progression of
periodontitis can be specified. Current knowl-
edge tells us that inducing periodontal patients
to stop smoking should be a higher priority
than genetic testing.
RISK FACTORS FOR PERIODONTITIS
Oral Hygiene, Plaque, and Microbiota
Although there is a clear causal relationship
between poor oral hygiene and gingivitis, the
relationship between oral hygiene status and
periodontitis is less straightforward. Good oral
hygiene can favorably influence the ecology of
the microbial flora in shallow to moderate
pockets, but it does not affect host response.
A simple but elegant study of experimental
human gingivitis conducted in the mid-
1960s134 showed the relation between plaque
deposits and gingivitis to be one of cause and
effect. Gingivitis is a nonspecific infection
caused by bacteria found in supragingival
plaque. There is less gingivitis in high-income
countries where good oral hygiene is a social
norm than in poorer societies where oral
hygiene activities are not a normal part of the
daily routine. There is also less calculus, both
supragingival and subgingival, as a result of bet-
ter oral hygiene and more professional dental
care. These differences are evident not only
between countries but also between the genders
and between socioeconomic strata within
the United States, as illustrated in Figs. 21-5 and
21-10, although subgingival calculus is seen to
be quite prevalent even among higher SES
American adults.
The presence of plaque and calculus
deposits is found to correlate poorly with
severe periodontitis in population studies,* and
the same is true for other measures of plaque
quantity.† What these studies of populations
*References 16,17,19,55,99,122,130,131,145,170.
†References 14,77,78,84,124,137,185.
with poor oral hygiene and little dental treat-
ment suggest is that, although gingivitis and cal-
culus deposition are more severe,7 the
prevalence and severity of periodontitis is not
all that different from conditions in developed
nations.15,76,187,188 Even among health profes-
sionals in the United States, oral hygiene prac-
tices seem unrelated to periodontitis.152
These poor correlations have all been
obtained using various measures of plaque
quantity (i.e., extent of plaque or calculus
deposits). Qualitative measures of plaque (i.e.,
specification of microbiota) have also produced
mixed results. In cross-sectional data, associa-
tions between putative periodontopathogenic
organisms and clinical periodontitis have been
reported,26,212 and the presence of these organ-
isms in subgingival plaque samples from suscep-
tible patients has predicted CAL over the short
term.85 On the other hand, the presence of spe-
cific microbiota could not predict the develop-
ment or progression of periodontitis in clinical
longitudinal studies of up to 3 years.126,127,244
It has long been understood that gram-
negative anaerobes and spirochetes are the main
putative pathogens in periodontal pockets, but
searches for the “cause” of periodontitis down
the years have not been able to discriminate well
between the various bacteria. More recently it
has become clearer that, within the broad spec-
trum of gram-negative organisms found at dis-
eased sites, several putative pathogens are
consistently found. The predominant group
includes Actinomyces actinomycetemcomitans,
Bacteroides forsythus, Porphyromonas gingivalis,
Prevotella intermedia, Fusobacterium nucleatum,
Campylobacter rectus, and Treponema denti-
cola.3,82,86,87,138,182,194,251 The presence of differ-
ent clonal types of these bacteria is recognized,
and it is not known whether all clonal types are
pathogenic. If they are not, that could well
account for some of the inconsistent associa-
tions found between the bacterial presence in
the periodontal crevice and clinical disease.180
Maintaining excellent oral hygiene affects
only the plaque and not the host response, one
reason why oral hygiene is not always effective in
controlling periodontitis. Still, practicing good
oral hygiene is a behavior whose value is sup-
ported by the evidence, mostly relating to the
conversion of supragingival plaque to subgingi-
val microfilm as discussed earlier in this chapter.

Local Factors
Cleaning under gingival overhangs is difficult,
and the growth of pathogenic flora can be
encouraged by inadequate hygiene. Although
gingival overhangs are common, they have been
found not to be associated with serious peri-
odontitis, at least not in young people.123
Although overhangs obviously should be
treated, local factors of this nature are generally
considered to be of minor importance in the eti-
ology of periodontitis compared to the nature
of the infection and the host response.175
Nutrition
Despite the centuries-old observation that sailors
suffering from scurvy (severe deficiency of ascor-
bic acid, or vitamin C) had bleeding gums, no
nutritional or dietary factors have been shown to
be directly related to the prevalence or intensity
of periodontitis. The possibility that generalized
malnutrition may influence its severity, however,
cannot be ignored.37,199 In the well-fed societies
of the high-income world, generalized malnutri-
tion is not a public health problem, although
malnutrition can be found in some individuals
with eating disorders. Ascorbic acid is probably
the nutrient most often thought to be a factor,
but it has been shown to be associated with peri-
odontitis only at the lowest levels of intake in the
United States, that is, 25% or less of the recom-
mended dietary allowance.101
A series of worldwide epidemiologic studies
in the 1960s, although they used the
Periodontal Index and lacked rigor in their
measurement of nutritional deficiencies, found
little evidence for a relationship between peri-
odontal disease and poor nutrition.197 These
studies were important at the time, but their rel-
evance today is questionable. Subsequent stud-
ies suggest that there may be an association
between more extensive gingival bleeding and
ascorbic acid deficiency,103,121 but whether such
a mechanism relates to bone loss or CAL is not
known. Nutritional adequacy is of course a pre-
condition for successful treatment of virtually
any disease, but there is no evidence to support
the use of ascorbic acid, or any other nutrient, in
the treatment of periodontitis.
Tobacco Use
Smoking is clearly a risk factor for periodontitis,
with relative risk on the order of 2.5-6.0 or even
21 Periodontal Diseases 273
higher.32 Exactly how smoking acts in the
causal chain, however, is still a subject of
research. Smoking was first identified as a
risk factor for periodontal diseases in an ana-
lysis of data from the first National Health
and Nutrition Examination Survey (NHANES I)
in 1971-74 in the United States,100 and the
evidence has continued to mount since
then.6,30,41,72,77,78,83,102,128 Assessments of ran-
domly chosen patient groupings invariably
show a higher prevalence of periodontitis
among smokers.81,89,106 It has been stated that
90% of persons with refractory chronic peri-
odontitis are smokers,107 and healing following
treatment is slower in smokers.79,109 Slower
healing could be due to the inhibition of
growth and attachment of fibroblasts in the
periodontal ligament of smokers and in their
slower posttherapy reduction of white blood
cells and neutrophils.45
Experimental studies of plaque accumula-
tion in smokers compared to nonsmokers have
given mixed results; some showed no differ-
ence,41,56,81 whereas others found more plaque
and calculus in smokers.158,181 Evidence on
whether smoking promotes the growth of peri-
odontal pathogens is mixed. Earlier studies
showed no difference in prevalence of these
bacteria subgingivally,189,215 but more recent
investigations suggest that smokers may have
higher prevalence, rather than higher counts or
proportions, of pathogenic species subgingi-
vally.83 Smoking appears to promote a favor-
able habitat for these species in shallow
pockets.63,83,241
Smoking suppresses the vascular reaction that
follows gingivitis and compromises host
response to infection in other ways. In experi-
mental plaque-induced gingivitis, although the
rate of plaque accumulation was equal in smok-
ers and nonsmokers, the increase in gingival vas-
cularity in smokers was only half of that seen in
nonsmokers.31 In effect, this is a masking of the
signs of inflammation.32 Further studies have
confirmed that smoking suppresses hemorrhagic
response as measured by bleeding on prob-
ing.29,33 Others have found no difference in the
extent of bleeding on probing between smokers
and nonsmokers, despite the fact that smokers
had deeper pockets240 or more plaque and calcu-
lus.181 In both instances more gingival bleeding
would have been expected in the smokers.
274 The Distribution of Oral Diseases and Conditions
With regard to other aspects of host response,
smoking inhibits granulocyte function,213 and
interactions between smoking and the IL-1 gene
cluster have also been indentified.151 In this
study, no difference in mean CAL could be
detected between smokers and nonsmokers
among those who were negative for the peri-
odontitis-associated genotype, but among those
who were positive for this genotype the smokers
had considerably greater CAL than nonsmok-
ers. Smoking aggravates all tissue-destructive
diseases, periodontitis included, by priming the
production of tumor necrosis factor-α ,80 and it
also causes the release of cytokines.66 Smoking
has been shown to be a stronger risk factor for
periodontitis than is insulin-dependent dia-
betes mellitus.155
In summary, the evidence is clear that smok-
ing is a major risk factor for periodontitis. The
first line of treatment for periodontitis should
always be to induce patients who smoke to quit
smoking.
Psychosocial Stress
Psychosocial stress seems to be associated with
progressive periodontitis, whether assessed in
a case-control study,52 cross-sectionally,69 or
in a longitudinal design.64 Because psychoso-
cial distress is a well-documented risk factor
for a number of different diseases,143 the iden-
tification of its predictive role in periodontitis
strengthens the hypothesis that periodon-
titis is related to systemic diseases. Our under-
standing of the mind-body connection in
periodontitis, as well as in other diseases, is
likely to expand and become more important
with time.
PERIODONTITIS AND SYSTEMIC
CONDITIONS
An emerging area of importance is that of the
potential link between periodontitis and some
serious systemic conditions. The periodontitis-
diabetes link is already well established. If oth-
ers become established, then prevention and
treatment of periodontitis will be seen in a com-
pletely different light. Here we look briefly at
the relationship between periodontitis and dia-
betes, human immunodeficiency virus (HIV)
infection, cardiovascular conditions, osteo-
porosis, and adverse pregnancy outcomes.
Diabetes
Both type 1 diabetes mellitus (type 1 DM, for-
merly called insulin-dependent diabetes melli-
tus) and type 2 DM (formerly called non-insulin
dependent diabetes mellitus) are risk factors for
periodontitis. There is good evidence to believe
that the most critical issue in managing peri-
odontitis in diabetic patients is the degree of
metabolic control achieved: generally, the
poorer the metabolic control, the more severe
the periodontitis.2,42,172,200,219,220,231 The con-
verse has also been proposed; that is, untreated
periodontal disease has been suggested to
diminish glycemic control and thus aggravate
diabetes.218
Younger adult patients with type 1 DM, espe-
cially those in whom the disease is of long dura-
tion, have more gingivitis and more deep pockets
than nondiabetic patients.59,68,92,203 No essential
difference in subgingival flora has been demon-
strated between diabetics and nondiabetics.
However, among diabetics mild periodontitis is a
risk factor for more severe diabetes, because dia-
betic patients have an exaggerated host response
to a given bacterial burden.202 Diabetic patients
with good metabolic control respond to conser-
vative treatment for periodontitis as well as do
nondiabetic individuals,46 and conservative treat-
ment can improve glycemic control in patients
with less well-controlled diabetes.214
Periodontitis also progresses more rapidly in
individuals with poorly controlled diabetes,208
and early age of onset of diabetes also is consid-
ered a risk factor for more severe disease.226
Persons with poorly controlled diabetes have
also been found to exhibit higher levels of the
enzyme β-glucuronidase in their gingival crevic-
ular fluid than do those in whom the disease is
well controlled.173
The most extensive studies among patients
with type 2 DM have been conducted in the
Gila River community in Arizona, where preva-
lence of type 2 DM is high. Patients with type 2
DM had substantially greater CAL, loss of alveo-
lar bone, and tooth loss.162,209 When age, gen-
der, and oral hygiene level all were controlled
for, type 2 DM was found to be associated with
a two to three times higher risk of developing
destructive periodontitis.65 This degree of risk is
similar to that found for severe CAL in diabetic
as compared to nondiabetic individuals in an
adult population in upstate New York.78

Studies of quantitative and qualitative
aspects of microflora in individuals with dia-
betes (both type I DM and type 2 DM) reveal no
notable differences between diabetics and non-
diabetics.222,254 Other suggested mechanisms
by which diabetes may contribute to periodon-
titis include vascular changes, polymorphonu-
clear leukocyte dysfunction, abnormal collagen
synthesis, cytokine production, and genetic pre-
disposition.34,54,108,115,172 Individuals with
poorly controlled diabetes have also been
shown to have impaired salivary flow.40
Periodontal treatment should always be a stan-
dard feature of health care for diabetic patients.
HIV Infection
It was the loss of immune response in acquired
immune deficiency syndrome (AIDS) that
focused attention on the relationship between
HIV infection and periodontitis. Most early
reports of this relationship came from cross-
sectional investigations studying convenience
samples of homosexual men, many of whom
were in late stages of the disease and severely
immunosuppressed.247,248 Most of these stud-
ies were not rigorously designed,195 so interpre-
tation of their results is uncertain. Studies of
the HIV-periodontitis link remain limited,
but those conducted with patients at earlier
stages of HIV infection, and especially with
patients receiving antiretroviral therapy, have
raised questions about the nature of the HIV-
periodontitis association.
Several studies examined the periodontal
condition of patients taking part in clinical tri-
als of the drug zidovudine (AZT). One reported
the periodontal health of patients in the early
stages of HIV disease to be generally good,62
and a longitudinal study of 30 HIV-positive
patients found a greater progression of peri-
odontitis over 18 months in this group than in
10 HIV-negative controls.253 However, in nei-
ther study was there analysis of periodontal dis-
ease in the patients taking AZT compared to the
others. In another follow-up of 114 homosexual
or bisexual men conducted over a period of 20
months, periodontal changes were found to be
related to HIV-1 serostatus, immune status, age,
and plaque deposits. The risk of CAL of 3 mm or
more over the 20 months was 6.16 times higher
in the more immunosuppressed patients
(CD4+ counts of less than 200/μl) than in the
21 Periodontal Diseases 275
less immunosuppressed patients, and this find-
ing was more pronounced in older subjects.22
HIV-positive patients showed a more sensitive
reaction to plaque than did the HIV-negative
patients. This study concluded that immuno-
suppression, especially in combination with
older age, was a risk factor for progression of
CAL and that seropositivity, independent of
immune status, was a risk factor for gingivitis.
In a cross-sectional study of HIV-positive
military personnel, however, the relation
between periodontal health and immune status
was less clear.216 A detailed follow-up of 474
patients from the same population, ages 18-49,
found CAL of 5 mm or more in 20% of the
patients. In this group, which was about 85%
male, neither the clinical stage of the disease
nor the CD4+ count was a good independent
predictor of severe CAL when account was taken
of other significantly associated variables (e.g.,
tobacco use).228
If HIV infection is really a risk factor for peri-
odontitis, we would expect to see an inverse
relation between severity of periodontitis and
CD4+ counts. The evidence is mixed, however,
except for those in the most severe stages of
AIDS. One early comparison between men at
different stages of HIV disease found little dif-
ference in terms of periodontal health.67 The
severity of periodontitis could not be related to
CD4+ counts in an HIV-positive group of
patients, none of whom was receiving antiretro-
viral therapy.144 Even in an African population
with no access to modern antiretroviral drugs,
periodontitis among HIV-positive individuals
was less prevalent and severe than had been
expected.205 The usual oral manifestations of
AIDS (candidiasis, hairy leukoplakia, Kaposi’s
sarcoma) were less common than expected in a
patient group receiving antiretroviral ther-
apy,217 and HIV-infected children whose disease
was under good medical control had no more
periodontal disease than did HIV-negative con-
trols.207 However, there are contrary findings as
well. HIV-positive patients in North Carolina
hospitals were found to have more severe peri-
odontitis than uninfected persons, and these
lesions were related to the degree of immuno-
suppression.149 A British study found more
periodontopathogenic bacteria in HIV-positive
patients than in HIV-negative controls,204 and
greatly increased numbers of mast cells and
276 The Distribution of Oral Diseases and Conditions
neutrophils were found in the gingival tissue of
HIV-positive patients.161 There are few reports
regarding levels of inflammatory cytokines in
HIV-positive persons, although one found more
total IL-1β in gingival crevicular fluid from HIV-
positive persons than in that from unaffected
persons.117
The microbiology of periodontitis in HIV-
positive persons relative to those not infected is
not clear, for both little difference159,160,192 and
significant differences154 have been reported.
None of these studies reported on the immuno-
suppression status of the subjects, although a
later assessment of HIV-positive patients found
the occurrence of necrotizing ulcerative peri-
odontitis to be related to decreasing CD4+
counts.70 Pathogenic bacteria have been
reported as no more frequent in HIV-positive
than in HIV-negative persons,221,232 although
the stage of immunosuppression of the patients
in these studies was not reported.
Our understanding of the relationship
between periodontitis and HIV/AIDS demands
further research, especially since the success of
highly active antiretroviral therapy has changed
the outlook on HIV infection (see Chapter 10).
Cardiovascular Disorders
Biomedicine’s recognition that chronic inflam-
mation anywhere in the body might affect heart
function12 has been a spur for research into the
way that periodontitis might affect cardiovascu-
lar disorders. An association between periodon-
titis and cardiovascular disorders has been
shown fairly consistently, although by no
means universally. The odds ratios have been in
the range of 1.5-3.0; if confirmed, this means
that periodontitis could be a causal factor of
some consequence in the top-ranked cause of
death in the United States. However, although
an association between these factors is evident,
cause and effect has not yet been demonstrated.
Cardiovascular diseases are complex, and the
research in this area has the challenge of disen-
tangling a maze of confounding and correlated
factors. Longitudinal studies with large num-
bers of participants are required to separate true
risk factors from this “background noise.”
Clinical trials of interventions, that is, tests to
see if periodontal treatment will reduce cardio-
vascular mortality, are also needed to establish
causality.
One report drawing on the NHANES I data-
base (1971-74) concluded that persons with
periodontitis at baseline had a 25% greater risk
of subsequent coronary heart disease than did
those without periodontitis.60 The risk was
especially strong for men under age 50 at base-
line. However, other analyses of the NHANES I
data set have found the opposite. Two studies
from the University of Washington (1) have
failed to demonstrate any significant associa-
tion between periodontal conditions and car-
diovascular disease94 and (2) have found that
the edentulous were at no greater risk of a car-
diovascular event than patients with periodon-
titis.95 Using the data from NHANES I, this
research group concluded that periodontitis
does not increase the risk of a bad cardiovascu-
lar outcome among those with preexisting heart
disease. They have also suggested that the asso-
ciations between chronic periodontitis and car-
diovascular conditions observed in smaller
studies can be attributed to insufficient statisti-
cal control for lifestyle differences.96 At the
same time, it must be recognized that NHANES
I recorded periodontal diseases by the now-
defunct Periodontal Index (see Chapter 16),
and this would tend to bias results toward
showing no effect. There is also reason to
believe that results can vary by the population
studied,146 which confirms the need for studies
involving large numbers and representative
samples. Self-reported periodontal conditions
were not a risk factor for cardiovascular disease
in a study of male physicians,90 whereas peri-
odontitis was related to self-reported heart con-
ditions in NHANES III.10
Circumstantial evidence supports an associa-
tion between periodontitis and cardiovascular
conditions. The presence of C-reactive protein is
a risk factor for cardiovascular disease, and the
protein has been found at higher levels in per-
sons with periodontitis both in clinical stud-
ies135,164 and in NHANES III.210 The NHANES
III data, interestingly enough, showed C-reac-
tive protein levels also to be high in edentulous
people, for reasons unknown.
If causality is to be established, the sequence
of events over time must be determined with
some confidence. (This is a drawback of cross-
sectional studies such as NHANES, because in
cross-sectional studies the exposure and the
outcome are both measured at the same time.

An example is when there is a follow-up of peo-
ple examined, as in NHANES I.) The results of
two studies using a retrospective cohort design
are helpful here. One was conducted in Canada,
where participants took part in a 1970-72
Nutrition Canada Survey that included a peri-
odontal assessment. The cardiovascular mortal-
ity of participants was assessed in 1993, and
significant associations were found between
subsequent death from cardiovascular disease
and (1) severe gingivitis at baseline and (2)
edentulism at baseline.157 The second study was
done in Sweden, where mortality experience
from 1970 to 1996 was assessed for 1393 partic-
ipants in a 1970 dental epidemiologic study.
Results of this study were essentially similar to
those of the Canadian study.104
It is interesting to note that what is being dis-
cussed here is essentially the “focal infection”
issue, which was first raised in 191197 and subse-
quently became the underlying rationale for
mass extractions over subsequent decades. The
focal infection theory faded in the 1950s, but its
underlying principle seems to have reemerged.
Osteoporosis
Osteoporosis is a condition of bone fragility char-
acterized by low bone mass and structural dete-
rioration. It is common in old age, especially in
postmenopausal women. Osteopenia is a less
severe form of bone-mineral loss. Because alve-
olar bone loss is often seen with generalized
osteoporosis, the question naturally arises as to
how much alveolar bone loss is actually due to
osteoporosis rather than to periodontitis. The
issues can also be stated as follows:43
●
Is generalized osteoporosis or osteopenia a
risk factor for periodontitis?
●
Does generalized osteoporosis or osteope-
nia lead to oral osteopenia?
●
Does periodontitis lead to oral osteopenia?
It can be seen from these questions that get-
ting the time sequence right in these slowly
developing conditions is an inherent research
problem, and that is probably the main reason
why these questions remain incompletely
answered.
Cross-sectional studies, not surprisingly,
give conflicting results. A number of studies
show an association between periodontitis and
low bone mineral density at various locations
in the body.98,111,196,223 However, other cross-
21 Periodontal Diseases 277
sectional studies have shown no association
between periodontitis and systemic bone min-
eral density measured at eight points in the
body245 and no difference in periodontitis lev-
els in postmenopausal women with osteoporo-
sis and in those without.136 A literature review
concluded that CAL was greater in osteoporotic
women than in nonosteoporotic women,
although the body of literature available for
review was rather sparse.114
Few longitudinal studies are available. One,
conducted in Denmark, followed 20 young peo-
ple with severe periodontitis over a 5- to 10-year
period. Mandibular bone mineral content was sig-
nificantly lower than bone mineral content else-
where in the body, which essentially indicates that
periodontitis is a local condition.242 The remain-
ing longitudinal studies were 1-2 years in duration
and focused on the effect of estrogen supplemen-
tation in postmenopausal women. Low estrogen
level is a factor in osteoporotic bone loss.
Estrogen-sufficient women in this study gained in
alveolar bone mineral density over a year, whereas
the estrogen-insufficient women experienced a
mean loss of bone.184 Estrogen supplementation
was also shown to reduce CAL in osteopenic and
osteoporotic women in early menopause.193
More research is clearly needed in this area.
Adverse Pregnancy Outcomes
The inflammatory mediators that are seen
in the periodontal diseases are the same ones
that play an important part in the initiation of
labor, so it is reasonable to hypothesize that
there are biologic mechanisms linking the two
conditions.246
A 1996 report concluded that mothers of
premature, low-birth-weight infants were about
7.5 times more likely to have periodontitis dur-
ing pregnancy than mothers of normal-weight
infants.168 A later case-control study conducted
by the same research group found that levels of
the inflammatory cytokine prostaglandin E2
were significantly higher in mothers who had
given birth to preterm low-birth-weight infants
than in mothers whose infants were of normal
birth weight.167 A later case-control study by a
different research group involving 448 women
found that those who had given birth to low-
birth-weight infants were four times as likely to
have high P. gingivalis–specific maternal serum
immunoglobulin G levels than did those who
278 The Distribution of Oral Diseases and Conditions
had infants of normal birth weight.57 However,
another case-control study found that the risk
of having a preterm low-birth-weight infant
decreased with increasing pocket depth; that is,
periodontitis appeared to be protective.58 This
finding is not easy to explain in light of the
other evidence.
Prospective studies are usually regarded as
stronger evidence than case-control studies
because the strength and extent of the exposure
can be measured more exactly. In a cohort of
1313 women, the risk of a preterm birth (35 or
fewer weeks’ gestation) was some five times
greater among women who had periodontitis at
21-24 weeks of pregnancy than among those
who did not.105 In another prospective study in
North Carolina, 19.9% of preterm infants
showed seropositivity for one or more peri-
odontal pathogens in fetal cord blood, com-
pared to 6.9% of full-term babies.140
Interim data from the first 814 deliveries in a
projected 5-year prospective study demonstrate
that the incidence or progression of periodonti-
tis during pregnancy is significantly associated
with a higher occurrence of preterm births.169
The conclusions of this study were strengthened
by the finding of a dose-response relationship:
greater severity of the periodontal conditions
was directly related to the increased risk of a
preterm low-birth-weight outcome.
The evidence favors an association between
maternal periodontitis and the risk of delivering
a preterm low-birth-weight infant. It is too early
yet to say that this link is causal, but it is strong
enough to indicate that periodontal monitor-
ing, and treatment when necessary, is a good
idea during pregnancy.
PREDICTION OF PERIODONTITIS
Attempts to identify predictors of future disease
go back some years. The aim is to identify the
presence of some easily measured entity, one
that clinicians can readily test for in a patient,
that will predict with high reliability the risk of
future disease. The research studies to identify
these predictors must have longitudinal designs
in which suspected predictors (e.g., plaque
deposits, subgingival calculus deposits, tobacco
use, diabetes, SES, specific cytokines in gingival
crevicular fluid, psychic stress) are measured in
participants at baseline, and development of
new periodontal lesions or progression of exist-
ing lesions is noted over a period of time. The
disease outcome can then be related to the base-
line measures. There are many complications in
this type of research given the complexity of the
host response to periodontal infections.18
Models that fit past data often cannot be accu-
rately extended to present conditions.252
The presence of visible plaque and calculus, as
one example of a hypothesized marker, was long
assumed to predict future CAL or bone loss, but
it is now seen that clinical measures of plaque
and calculus by themselves do not predict future
disease to any useful extent.14,47,85,118,186 Models
that have included the subgingival presence of
specific pathogens like A. actinomycetemcomitans,
P. intermedia, P. gingivalis, and B. forsythus along
with other indicators have shown a moderate
degree of predictive value.25,138,227,230 Host
response must be worked into the equation, and
it is now recognized that smoking and genetic
predisposition are major players in this regard.
When smoking and periodontitis-associated IL-1
genotype status (positive or negative) were
included in a predictive model, none of the base-
line clinical indicators added significantly to the
ability of the model to predict subsequent tooth
loss. The baseline clinical indicators performed
much better in a model that included IL-1 geno-
type status in nonsmokers.148 What this body of
research has demonstrated is that multiple pre-
dictors work better than any single predictor by
itself, and the nearest we can get to a universal
predictor is tobacco use.5,25,139,165
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 22 Dental Fluorosis
PREVALENCE OF FLUOROSIS IN THE UNITED
STATES
RISK FACTORS FOR DENTAL FLUOROSIS
Fluoridated Drinking Water
Fluoride Dietary Supplements
Dental fluorosis is a permanent hypomineral-
ization of enamel that is characterized by
greater surface and subsurface porosity than in
normal enamel and that results from exposure
of the immature tooth to excess fluoride (F)
during developmental stages. Preeruptive
enamel maturation consists of an increase in
mineralization within the developing tooth and
a concurrent loss of early-secreted matrix pro-
teins. Excess F available to the enamel during
maturation disrupts mineralization and results
in excessive retention of enamel proteins.5
Fluorosis is thought to result from the
unerupted tooth’s constant exposure to elevated
plasma F concentrations rather than from peri-
odic spikes in F concentration.69 Although suf-
ficiently high F concentrations might affect
enamel at all developmental stages,15 early
preeruptive maturation appears to be the time
when enamel is most sensitive to the effects of F,
both in animals16,53 and in humans.19 Elegantly
designed human studies have suggested that this
critical period for the development of fluorosis
in the human maxillary permanent central inci-
sor begins around the age of 22 months and
extends for periods of up to several years after
that for later-developing teeth.19
In its mildest forms, fluorosis appears as
barely discernible fine, lacy markings that fol-
low the perikymata across the width of the
enamel surface. At this very mild level, fluorosis
can be detected only by an experienced dental
examiner. At the opposite extreme, the most
Early Use of Fluoride Toothpaste
Infant Formula
DENTAL FLUOROSIS AND CARIES
DENTAL FLUOROSIS AS A PUBLIC HEALTH
PROBLEM
severe forms of fluorosis manifest as heavily
stained, pitted, and friable enamel that can
result in loss of dental function. Fluorosis is a
dose-response condition; gradations between
these two extremes range from more obvious
white, lacy markings to a nontranslucent white
coloration of the whole enamel surface. The
brown stain that often accompanies moderate
fluorosis is a posteruptive feature that results
when certain dietary ingredients are picked up
by proteins in the porous outer enamel21; it is
seen only when porous enamel has formed
prior to eruption.
Fluorosed surface enamel contains higher F
concentrations than does unaffected enamel,
and the F enamel content increases with the
severity of the condition.52 Teeth that mineral-
ize later in life generally show more severe fluo-
rotic disturbances than do those that mineralize
earlier.3,35-37 Fluorosis is less common in the
primary than in the permanent dentition,
although fluorosis of the primary teeth does
occur.66,67 It is common in the primary denti-
tion in high-F areas of the world, such as East
Africa.34,45,46,62
Because dental fluorosis is a dose-response
condition, the higher the F intake during the
critical period of tooth development, the more
severe the fluorosis.14,17,35 The threshold, if
indeed there is one, is low: 0.03-0.1 mg F/kg
body weight has been suggested as the border-
line zone,22 at least for European children.
Because that range encompasses the so-called
287
288 The Distribution of Oral Diseases and Conditions
optimum intake range of 0.05-0.07 mg F/kg
body weight per day (Chapter 24), it is not
clear whether other factors (e.g., nutrition) lead
to these differences in estimates or whether
they merely reflect biologic variation. Studies
in Kenya have found fluorosis with average
intakes as low as 0.04 mg F/kg body weight.3
Certainly a range of fluorosis severity is seen
among individuals who appear to have similar
exposures to F.
In those parts of the world where severe fluo-
rosis is endemic, such as some regions of Africa,
the condition can be seen when F levels in drink-
ing water are low,18 so that other, unknown
exposure sources must be present. In other cases
it occurs with ingestion of certain foods known
to be high in F.70 Studies in such localities have
increased our understanding of fluorosis, but
the living conditions in those areas differ greatly
from those in the United States and other high-
income countries.
PREVALENCE OF FLUOROSIS
IN THE UNITED STATES
Fluorosis in the United States was first mapped
by Dean during his classic studies of the 1930s
and early 1940s. These studies are discussed in
Chapter 24; they are an integral part of the story
of how fluorosis and caries experience were first
associated with F concentrations in drinking
water.
One part of the United States that received a
lot of attention from Dean was northern
Illinois, where there is an extensive belt of natu-
rally fluoridated drinking water. Seven of these
communities, with water naturally fluoridated
to varying degrees, were revisited by researchers
from the National Institute of Dental and
Craniofacial Research (NIDCR) in 1980, in
1985,27 and again in 1990.56 Relating age to
fluorosis and tooth calcification, the NIDCR
team concluded that F intake had increased dur-
ing 1970-77 but had not increased subse-
quently. The 1990 follow-up found that the rise
in age-standardized fluorosis prevalence
observed in the optimally fluoridated areas over
1980-85 did not continue during 1985-90. At
above-optimum water F concentrations, fluoro-
sis either remained stable or showed no sus-
tained increase over the decade between 1980
and 1990.
100
80
60
Percent
40
20
0
1930s 1990s 1930s 1990s
Fluoridated areas Nonfluoridated areas
Fig. 22-1 Increase in dental fluorosis prevalence in North
America since initial studies in the 1930s. The bars represent
the prevalence ranges reported in Dean’s studies and in those
after 1990.12,14
Although there are difficulties in comparing
data obtained 60 years apart, it is clear that the
prevalence of dental fluorosis in the United
States has increased since the time of Dean.12,60
Prevalence among children was reported to be
22.3% in the 1986-87 National Survey of
Dental Caries in U.S. School Children, ranging
by age from 18.5% of 17-year-olds to 25.8% of
9-year-olds.7 This higher prevalence in the
younger children hints that prevalence might
still be increasing. Almost all of the fluorosis
recorded in the 1986-87 survey was mild or
very mild. Although there is little firm evi-
dence, a slight increase in fluorosis severity
may have accompanied the large increase in
prevalence.63
The largest relative increase in fluorosis since
Dean’s time has been seen in nonfluoridated
areas (Fig. 22-1), which suggests that the F expo-
sure from sources other than drinking water is
driving the increase in fluorosis prevalence.
RISK FACTORS FOR DENTAL
FLUOROSIS
Because fluorosis is a disturbance of enamel due
to excessive F intake during the developmental
period, risk factors are related to the ingestion
and absorption of F at the critical periods of

preeruptive tooth development. Age is a demo-
graphic risk factor in that fluorosis can only
occur with preeruptive F exposure. There is no
evidence for racial or ethnic differences, and
socioeconomic status (SES) is a demographic
risk factor only to the extent that F exposure
from toothpaste and infant formula may vary
by SES. There is no reason to believe that the use
of F mouthrinses and the presence of profes-
sionally applied gels and varnishes are risk fac-
tors for fluorosis, although obviously the
protocols for application of these products
must be designed to minimize ingestion.
Fluoridated Drinking Water
Drinking fluoridated water is a minor risk factor
for fluorosis. It was documented long ago that
in the United States, even at around 1.0 parts
per million (ppm) F, 7%-16% of children born
and reared in areas with fluoridated water
exhibit mild or very mild dental fluorosis in the
permanent dentition.1,14,55 This degree of
prevalence was recorded at a time when drink-
ing water was virtually the only source of expo-
sure to F, and prevalence has risen relatively
more in the nonfluoridated areas since
then.33,56 Even small changes in F concentra-
tions in drinking water can lead to considerable
change in fluorosis prevalence.20,61
Fluoride Dietary Supplements
F dietary supplements, in the form of tablets,
drops, or F-vitamin combinations, have been
used for years in nonfluoridated areas to pre-
vent caries (see Chapter 26). Regardless of the
role of F supplements in preventing caries, there
is strong evidence that supplements are a risk
factor for mild to moderate fluorosis. Case-
control studies in nonfluoridated areas of New
England found that exposure to F supplements
during the first 6 years of life, together with
higher SES, significantly increased the risk of
developing fluorosis.48,50 Later research, as
would be expected, found the risk to be
extremely high when supplements are used
(inappropriately) in fluoridated areas.49 Other
studies have demonstrated the link between use
of supplements and fluorosis risk,2,32,34,51 and F
supplementation was later confirmed as a risk
factor for fluorosis in a comprehensive system-
atic review.29 It was this evidence that led the
American Dental Association in 1994 to reduce
22 Dental Flurosis 289
the recommended F supplement dosage for
caries prevention in children (see Chapter 26).
Early Use Of Fluoride Toothpaste
Young children in whom the swallowing reflex
is not yet fully developed can ingest up to 0.3-
0.5 g of toothpaste (0.3-0.5 mg F) at each brush-
ing.4,6,25 These findings naturally raise the issue
of whether overzealous use of F toothpaste in
young children is a risk factor for fluorosis. One
study of a Toronto area with fluoridated water
found that early use of F toothpaste (before 2
years of age) and prolonged use of infant for-
mula produced with fluoridated water were
strong risk factors for the later development of
fluorosis.47 Although most of the fluorosis seen
in that Toronto study was very mild, later stud-
ies were able to confirm a clear risk of fluorosis
with early use of F toothpaste.* The risk from
early use of F toothpaste, however, was usually
not as high as that seen with F supplements.
Infant Formula
Use of infant formula has been recognized as a
risk factor for fluorosis, both because of its own
F content and especially because it may be
mixed with fluoridated water.47,49 Soy-based
formulas contain higher F concentrations than
do milk-based formulas.30,41
DENTAL FLUOROSIS AND CARIES
Dean’s studies in the 1930s and 1940s found
that caries experience dropped sharply as the
F concentration of drinking water rose from
negligible to 1.0 ppm and that it tended to level
off after that (see Chapter 24). But when F con-
centration reaches a point at which severe fluo-
rosis is common and the enamel of affected
individuals becomes friable and liable to frac-
ture, caries experience has been observed to
increase.23 This phenomenon was demon-
strated in the United States by the NIDCR stud-
ies in the seven communities in northern
Illinois in 1980, 1985, and 1990 described ear-
lier.56 The results of the caries examinations in
relation to several F concentrations in drinking
water are shown in Fig. 22-2. Data for each year
describe a u-shaped curve: with increasing
F levels, caries experience diminishes to a cer-
*References 32,34,40,42,49,54,57.
290 The Distribution of Oral Diseases and Conditions

4 tain point and then starts to rise again. Dean

1980 showed that caries experience in the 1930s con-
1985
tinued to drop for water F levels at least as high
as 2.6 ppm;13 unfortunately he did not publish
1990
caries data from the communities with higher
water F levels he studied earlier in his career.
Mean DMFS

Fig. 22-3 shows the relation between caries

2 experience and water F levels, age standardized
and restricted to data for permanent residents,
among participants ages 5-17 in the 1986-87
National Survey of Dental Caries in U.S. School-
children. It makes an interesting comparison
with the corresponding data from Dean’s studies
(see Fig. 24-1); the absolute caries levels are
0 much lower in Fig. 22-3, and there is a less pro-
Optimum 2X 3X 4X
Optimum Optimum Optimum
nounced association between caries and water F
levels. These two factors together indicate the
Community water fluoride level importance of F exposure from sources other
Fig. 22-2 Decayed, missing, and filled tooth surfaces than drinking water that has taken place since
(DMFS) in children in seven Illinois communities by level of Dean’s time. Fig. 22-4 shows fluorosis preva-
fluoride in the drinking water in 1980, 1985, and 1990. Data lence data from the same national survey, and
are age-adjusted for comparability.56 here fluorosis seems to fall into three groups: the
lowest prevalence from 0 to 0.5 ppm F, a plateau
from 0.6 to 1.2 ppm F, and the highest preva-
lence at 1.3 ppm F and above.

3
Mean DMFS

0
0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1 1.1 1.2 1.3 1.4 1.5 1.6+

Water fluoride levels (ppm)

Fig. 22-3 Decayed, missing, and filled tooth surfaces (DMFS) in children ages 5-17 by fluoride level in the drinking
water. Age-adjusted data for permanent residents from the 1986-87 National Survey of Dental Caries in U.S.
Schoolchildren.28

60
50
40
Percent
30
20
10
0
0 0.1 0.2 0.3 0.4 0.5
Fig. 22-4 Fluorosis prevalence among children ages 7-17 years by fluoride level in the drinking water. Age-
adjusted data for permanent residents from the 1986-87 National Survey of Dental Caries in U.S. Schoolchildren.28
Caries could increase with higher F levels in
drinking water either because restorative treat-
ment is sought for fluorosed enamel or because
pitted and friable enamel is diagnosed as caries.
Although friable enamel can certainly lead to
loss of function and require dental restoration,
it is not caries. However, it is possible that bro-
ken enamel makes a tooth more vulnerable to
caries. Whatever the link, severe fluorosis is
obviously a condition to be avoided.
DENTAL FLUOROSIS AS A PUBLIC
HEALTH PROBLEM
At what point does dental fluorosis become a
public health problem? There is no reason to
call it such in a community where it is found
only in its mildest forms, even in U.S. commu-
nities where prevalence is around 50% in chil-
dren. On the other hand, its high prevalence
and severity make it a public health problem in
the countries of East Africa9,38,39,44,46,65,68 and
in parts of India.8,59 It is an urgent problem in
those regions of Ethiopia and India where skele-
tal fluorosis, which can be a debilitating condi-
tion, is found.24,31
22 Dental Flurosis 291
0.6 0.7 0.8 0.9 1 1.1 1.2 1.3 1.4 1.5 1.6+
Water fluoride levels (ppm)
The relatively greater increase in fluorosis
prevalence in nonfluoridated communities,
compared to fluoridated areas (see Fig. 22-1),
must be attributable largely to an increase in F
ingestion from sources other than drinking
water. The risk of fluorosis from dental prod-
ucts, notably toothpaste and F supplements,
was described earlier, and F ingestion can be
higher than expected from soft drinks and fruit
juices processed with fluoridated water. For
most people, drinking water is now just one of
numerous exposures to F.
Dental fluorosis cannot be classed as a public
health problem in the United States and other
countries where controlled water fluoridation is
extensive. It would be a mistake, however, to
assume that it cannot become so. There is evi-
dence from several parts of the world that peo-
ple are quite aware of even the milder forms of
fluorosis in their teeth.10,11,26,43,54,58 If high-F
toothpastes become widely marketed, and if the
esthetic standards of the public regarding fluo-
rosis become more stringent, then dental and
public health authorities could be faced with
demands to do something about it. This could
include restricting exposure to F, so that possi-
292 The Distribution of Oral Diseases and Conditions
bility is best avoided by prudent use of F now.
The U.S. Public Health Service recommenda-
tions64 on use of F are a good place to start.
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31. Jolly SS, Singh BM, Mathur OC, Malhotra KC.
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46. Olsson B. Dental findings in high-fluoride areas
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 23 Oral Cancer and Other Oral
Conditions
ORAL CANCER
Occurrence and Distribution
Risk Factors
Dental Professionals and Oral Cancer
With the decline in dental caries among chil-
dren and the understanding that severe peri-
odontal diseases are not as common as once
thought, dental professionals are in a position
to spend more time on the diagnosis and treat-
ment of conditions that traditionally have not
occupied much time in the dental office. This
chapter looks at the distribution of some of
these conditions and at the risk factors and risk
indicators associated with them.
ORAL CANCER
Occurrence and Distribution
Of all conditions that dental professionals see
and treat, oral cancer is the one that literally has
life and death implications. Age-adjusted oral
cancer mortality rates among males in the
United States have shown a long-term reduc-
tion, most notably since the mid-1980s
(Fig. 23-1). Mortality rates among American
females, which have always been low, have
shown only slight reduction over the 24-year
period covered in Fig. 23-1.
The term oral cancer includes disease category
numbers 140-149 of the International
Classification of Diseases, ninth revision,
known as ICD-9.33 This group includes cancers
of the lip, tongue, buccal mucosa, floor of the
mouth, salivary glands, and pharynx. It does
not include throat cancer. The occurrence of
oral cancer and its site distribution within the
mouth varies widely in different parts of the
world,61,65 presumably because of the environ-
294
OTHER SOFT TISSUE LESIONS
CLEFT LIP AND PALATE
MALOCCLUSION
TEMPOROMANDIBULAR JOINT DISORDERS
mental factors with which these cancers are
associated. Squamous cell carcinomas of the
oral mucosa, tongue, and lip comprise 80% of
all oral cancers on a global basis.34
In 2004 there were approximately 28,300
new oral cancer cases in the United States and
some 7200 deaths from oral cancer. Table 23-1
shows the extent of oral cancer in the United
States and compares incidence data for 2004
with that for 1988. There were more new cancers
of all kinds in 2004 than in 1988, but the num-
ber of new oral cancers had actually dropped. As
shown in the table, cancers of the oral cavity
constituted some 2.1% of all new cases reported
in 2004, down from 3.1% in 1988. Mortality
from oral cancer has also dropped, both in
absolute numbers and proportionately, and
accounted for 1.3% of all cancer deaths in 2004.
The proportionate drop in mortality rates is
attributable both to the slight drop in absolute
numbers of oral cancers and to the absolute
increase in mortality from other types of cancer.
Although these overall trends in the United
States are moving in the right direction, oral
cancer remains twice as prevalent in males as in
females (see Table 23-1), and annual incidence
among males in 1992-99 remained more
than twice the rate seen in females (Fig. 23-2).
Twice as many deaths from oral cancer occur in
males as in females. Some differences between
the races are seen in the specific sites within the
oral cavity in which oral cancer is found (Table
23-2), and there are no obvious explanations
for these differences.
 23 Oral Cancer and Other Oral Conditions 295

8
Female

Age-adjusted deaths/100,000 population

7
Male

0
1976 1979 1982 1985 1988 1991 1994 1997 2000

Years

Fig. 23-1 Age-adjusted mortality from oral cancer per 100,000 population for males and females in the United
States, selected years 1976-2000.84

Table 23-1 New cancer cases and deaths, by gender, for all cancers and for oral cancers, United States, 1988
and estimated for 20042,76
Site Year Total Males Females

New Cases (Incidence)

All cancers (thousands) 1988 985 495 490
2004 1368 700 668
Oral cancers (thousands) 1988 30.2 20.5 9.7
2004 28.3 18.6 9.7
Oral cancers as percentage of all cancers 1988 3.1 4.1 2.0
2004 2.1 2.7 1.5

Deaths
All cancers (thousands) 1988 494 263 231
2004 564 291 273
Oral cancers (thousands) 1988 9.1 6.0 3.1
2004 7.2 4.8 2.4
Oral cancer deaths as percentage of all cancer deaths 1988 1.8 2.3 1.3
2004 1.3 1.6 0.9

Oral cancer is closely related to older age was 5.2 per 100,000, nearly double the rate of 2.7
(Fig. 23-3), and peak age for mortality from oral in whites.82 However, by 2000, mortality among
cancer comes earlier for African-Americans than African-Americans had dropped to 4.1 per
it does for whites. Overall annual mortality 100,000 and mortality among whites to 2.5 per
among African-Americans in the 1988-92 period 100,000.85 Mortality is most likely related to low
296 The Distribution of Oral Diseases and Conditions

80
Female
Male

Incidence per 100,000 population

60

40

20

0
25-29 35-39 45-49 55-59 65-69 75-79 85+

Age-group

Fig. 23-2 Annual incidence of oral cancer per 100,000 population by age and gender in the United States,
1996-2000.85

Table 23-2 Site of occurrence of oral cancer for estimated new cases per 100,000 population, for all races,
whites, African-Americans, and Asians/Pacific Islanders, United States, 200085
Primary Site All Races Whites African-Americans Asians/Pacific Islanders

All cancers 464.2 462.7 464.0 298.2

All oral cancers 10.4 10.3 10.8 8.3
Lip 0.8 0.9 0.1 Negligible
Tongue 2.6 2.6 2.1 1.6
Salivary glands 1.2 1.2 0.7 0.9
Floor of the mouth 0.8 0.7 1.1 0.4
Gum and other mouth sites 1.6 1.6 1.8 1.2
Pharynx 3.2 3.0 4.3 3.9
Other sites 0.4 0.3 0.6 Negligible

socioeconomic status in the United States, as it finding attributed to increasing alcohol con-
has been shown to be in Britain.64 sumption4 and to social deprivation.47
A standard measure of cancer severity is the The prospects for survival are considerably
5-year relative survival rate, which is the per- higher if diagnosis is made when the cancer is
centage of people still alive 5 years after diagno- confined to a local lesion, rather than when
sis, adjusted for those who died for some other there is regional or distant spread (Table 23-3).
reason over the 5 years. Fig. 23-4 shows these Five-year survival is four times greater when
rates for men and women from 1974 to 1999, tumors are diagnosed at localized stages rather
and it is evident that they have not changed than after metastasis has occurred. It follows
much. Survival rates are much more favorable that cancers and precancerous lesions should be
for whites than for African-Americans, and the diagnosed as early as possible if treatment is to
disparity in survival rates between the races have a good prognosis, but there is nothing in
clearly had not improved by the turn of the cen- the data to suggest that the proportion of oral
tury (Fig. 23-5). Survival rates have diminished cancers diagnosed at earlier, more localized
in poorer parts of Europe over recent years, a stages has increased since 1973.82
 23 Oral Cancer and Other Oral Conditions 297

20
White
18
African-American
16

Deaths per 100,000 population

14

12

10

0
30-34 40-44 50-54 60-64 70-74 80-84

Age-group

Fig. 23-3 Mortality from oral cancer per 100,000 population by age and race in the United States, 1996-2000.85

70
Female
60 Male

50

40
Percent

30

20

10

0
1974-76 1977-79 1980-82 1983-85 1986-88 1989-91 1992-99

Years

Fig. 23-4 Five-year relative survival rates for males and females diagnosed with oral cancer in the United States,
1974-99.1,85

Risk Factors various forms.65 For example, in India some

Worldwide, the combination of tobacco use, 30%-40% of all reported cancers are oral can-
heavy alcohol use, and poor diet is responsible cers,3,16 a remarkably high prevalence that is
for 90% of all oral cancers.35 The single risk closely associated with several forms of tobacco
factor most consistently associated with oral can- smoking and chewing in that country. Elsewhere,
cer on a global basis is the use of tobacco in its smoking and other uses of tobacco are the most
298 The Distribution of Oral Diseases and Conditions

70
White
60 African-American

50

40
Percent

30

20

10

0
1974-76 1977-79 1980-82 1983-85 1986-88 1989-91 1992-99

Years

Fig. 23-5 Five-year relative survival rates for whites and African-Americans diagnosed with oral cancer in the
United States, 1974-99.85

Table 23-3 Five-year survival rates for whites and
African-Americans diagnosed with oral cancer by stage
of metastatic spread from the primary site, United
States, 1992-9985
Localized Regional
(%) (%)
Whites 82.7 49.9
African-Americans 68.8 30.6
consistently identified risk factors. High relative
risks in the range of 6:1 to 14:1 for the develop-
ment of oral cancers in smokers compared to
nonsmokers continue to be reported in a num-
ber of countries.20,21,36,51,53,60,80 The risk of
developing oral cancer from smoking is just as
high for women as for men,37 and risk dimin-
ishes with time since quitting.21,53 The risk
of oral cancer in association with smoking is
greatest for pharyngeal cancers and lowest for
lip cancer.51
The extraordinarily high prevalence of oral
cancer in India has naturally attracted research
attention, especially in light of the widespread
habit of chewing the areca nut (betel) in that
country. Betel is usually chewed in a mix with
tobacco, and lime and other ingredients are
sometimes added. Some studies concluded that
the cancer risk comes largely from the tobacco
with little role for betel.28 However, other
research has identified betel as a major etiologic
factor in the development of oral submucous
Distant fibrosis,58,83 a precancerous condition that has
(%) a high rate of malignant transformation.58,77
Nodular leukoplakia, a precancerous condition
26.7 that may be associated with oral submucous
21.5
fibrosis, also shows a high rate of malignant
transformation. Tobacco users with nodular
leukoplakia are at especially high risk of oral
cancer.26 Intervention studies to curtail tobacco
and betel chewing have had moderate success in
reducing leukoplakia formation in India and
confirm that chewing tobacco and betel are
major risk factors for oral cancer.27
Over recent years, the resurgence in the use of
smokeless tobacco has presented the United
States with another risk factor for oral cancer.
Because this recent increase in use is predomi-
nantly among young people,11 it has so far had
little impact on incidence and mortality data, but
if widespread use continues, the incidence of oral
cancer could rise sharply in the years ahead. The
dimensions of smokeless tobacco use, its effects
on human health, and what dental professionals
can do about it are discussed in Chapter 30.
Alcohol consumption, especially heavy con-
sumption, has also been identified as a risk

factor, although not all studies have found it to
be a risk factor independent of tobacco use.53,80
The role of genetics in oral cancers is likely to
be strong, although it requires further defini-
tion at present. Although mutation of the p53
cancer-suppression gene has been recognized as
an etiologic factor in many forms of cancer for
some years, its role in oral cancer is only starting
to be well defined.41,63 Further research in oral
cancer is likely to focus on the genetic influ-
ences and molecular risk markers, but the
importance of reducing the most common risk
factors still remains.
Other risk factors have been identified,
although the evidence is less consistent than it
is for smoking and alcohol use. Painful and ill-
fitting dentures are still often listed as a risk fac-
tor,95 although supportive evidence is lacking.
Long-term exposure to strong sunlight is seen as
a risk factor for lip cancer; however, aside from
the higher prevalence in sunnier climates, evi-
dence for that contention is not easy to find.79
Chronic inflammation, such as that found with
lichen planus, has also been suggested as a pos-
sible risk factor.14
Dental Professionals and Oral Cancer
In terms of diagnosis, concern has been
expressed that survival rates for oral cancer are
unnecessarily low because of delays by patients
in seeking attention for lesions and because of
delays in diagnosis by health professionals.25
Dentists and hygienists must be sensitive to the
presence of leukoplakia and other precancerous
conditions, especially in patients who present
with known risk factors in their histories.
Leukoplakia has long been known as a precan-
cerous condition, meaning that it has been doc-
umented to precede the development of cancer.
It has also been pointed out that mucosal ery-
throplakia, rather than leukoplakia, is often the
first sign of cancerous change in a lesion.51
A related issue here is the unusually high rate of
second primary cancers among patients who
have previously had oral cancer, a finding that is
also correlated with higher tobacco use and
alcohol consumption.12
OTHER SOFT TISSUE LESIONS
In general, the epidemiology of soft tissue
lesions other than cancer has not been well
23 Oral Cancer and Other Oral Conditions 299
studied. Precancerous conditions are obviously
the lesions of most concern. A precancerous
lesion is defined as morphologically altered tis-
sue in which cancer is more likely to occur than
in its apparently normal counterpart.93 The
principal precancerous conditions for oral can-
cer are generally recognized as leukoplakia and
erythroplakia.
Leukoplakia, already mentioned as a risk fac-
tor in tobacco users, is generally defined as a
white patch or plaque that cannot be character-
ized clinically or by pathologic examination as
anything else,42,89 a definition by default that is
not very satisfactory. There is no general figure
for the prevalence of leukoplakia in the popula-
tion; it has been studied only in connection
with known cancer risk factors such as smoking.
The rate of transformation of leukoplakia
lesions into oral cancer varies in different
parts of the world but is generally on the
order of 6%.81
Erythroplakia is a bright red or velvety plaque
that cannot be characterized clinically or patho-
logically as being due to anything else,93
another definition by default. When these
lesions are found, or even suspected, immediate
biopsy is called for and referral to an oral
pathologist is recommended.
In general, little is known about the distribu-
tion of other soft tissue conditions, including
papillary hyperplasia, candidiasis, pemphigus
and pemphigoid, and lichen planus, or about
the prevalence of herpes infections. Not surpris-
ingly, risk factors have not been defined for
these conditions (except that papillary hyper-
plasia is associated with ill-fitting dentures).
There is a clear need for some basic epidemio-
logic research on all of these poorly understood
conditions.
CLEFT LIP AND PALATE
The occurrence of cleft lip, cleft palate, or both
in the United States each year was estimated
some years ago as approximately 1 in 700 live
births.23 There is nothing to suggest that the rate
has changed since then. Clefts are predomi-
nantly of genetic origin, and there is evidence
of genetic-environmental interactions in their
etiology.8,32,45,57,75
Attempts to isolate some of the potential envi-
ronmental risk factors and the gene-environment
300 The Distribution of Oral Diseases and Conditions
interactions have proved difficult. Even the data
on maternal smoking as a risk factor is inconsis-
tent,9,38,44,91,94 which seems odd considering the
ubiquity of smoking as a risk factor for just about
everything. There may be an interaction between
maternal smoking during pregnancy and the
infant’s genotype.32,75
Maternal age seems not be a demographic
risk factor,88 and there also appears to be
no link with socioeconomic status.7 Among
various ethnic groups in the United States, the
lowest reported prevalence is among African-
Americans and the highest is among persons of
Japanese ancestry.24 A correlation has been
reported between late birth order and presence
of clefts.87
Although problems with these studies
are recognized, epidemiologic correlations
reported from several studies24,69,72 are the
following:
●
More facial clefts are found in boys, but
more isolated cleft palates are found in
girls.
●
Cleft lip and palate appear more frequently
in plural births than in single births.
●
Babies with clefts generally are of lower
birth weight, and an association has been
found between clefts and prematurity.
There is a higher infant mortality rate
among children born with clefts,31 and 35%
of those born with clefts have associated
malformations. The higher mortality rate is
attributed more to these associated malfor-
mations; clefts without associated mal-
formations do not present an increased risk
of infant mortality.19
The occurrence of clefts is also associated
with the following:
●
Threatened spontaneous abortion during
the first and second trimesters of pregnancy
●
Influenza and fever in the first trimester
●
Maternal drug use during the first trimester
The small number of studies on clefts means
that the probability that the reported correla-
tions are due to chance is moderately high. As a
result, more study is needed to confirm the
associations described.
MALOCCLUSION
The difficulties of quantifying malocclusion
were described in Chapter 18. Differing cultural
perceptions of what constitutes a malocclusion,
differing perceptions of malocclusion on the
part of orthodontic specialists and general den-
tists, and difficulties in achieving a sufficient
degree of examiner consistency in use of maloc-
clusion indexes all make summary statements
difficult.
Malocclusion was measured on a nationally
representative sample of U.S. youths ages 12-17
in the 1966-70 National Health Examination
Survey.86 This survey employed the Treatment
Priority Index (see Chapter 18), and results
showed that a higher proportion of African-
American youths than white youths had either
normal occlusion or only minor malocclusion.
There was little difference in malocclusion
between young white males and females; how-
ever, a notably higher proportion of African-
American females than of African-American
males had very severe malocclusion. Some
occlusal traits were later measured in the third
National Health and Nutrition Examination
Survey (NHANES III, 1988-94), although no
attempt was made to craft them into an index.
The conditions recorded were diastema of more
than 2 mm, alignment of lower and upper
teeth, posterior crossbite, overbite, and overjet.5
A 1985 review of the prevalence of malocclu-
sion in the United States52 concluded that good
epidemiologic evidence existed that there were
significant departures from “normal occlusion”
in American children and that a majority of
American children “would benefit from ortho-
dontic treatment.” Unfortunately that conclu-
sion remains as problematical as it always was,
because normal occlusion was not defined, and
in fact the authors seemed to be referring to
ideal occlusion. Whether these children would
really benefit, or whether orthodontic treat-
ment would make no difference to their oral
status, must remain a matter of conjecture.
TEMPOROMANDIBULAR JOINT
DISORDERS
Disturbances of the temporomandibular joint,
usually referred to as temporomandibular joint
dysfunction (TMD) or temporomandibular
pain and dysfunction syndrome (TMPDS), are a
group of extremely painful and distressing con-
ditions. Diagnosis is not easy because TMD is
often accompanied by generalized pain in the

head and neck region. There is no agreement on
what constitutes standard treatment proce-
dures, and treatment outcomes are mixed.18 It is
hardly surprising that the epidemiology of these
conditions is poorly understood.10,13
The difficulty in defining risk factors in TMD
stems from the absence of a suitable case defini-
tion of TMD. To put the problem in perspective,
the disagreements on criteria for judging the
presence of caries (see Chapter 15) exist over
only a narrow range of clinical detection of an
agreed-upon pathologic condition. The prob-
lems in defining TMD conditions, however, go
far beyond these relatively restricted defini-
tional problems; they are more akin to the
problems in measuring malocclusion. When a
condition cannot be defined, valid measure-
ment is virtually impossible. Definitions of
TMD exist,67 but they tend to be all encompass-
ing and nonspecific, and hence not of much
operational value for research or treatment pur-
poses. Conferences on TMD have generally
agreed that a case definition should include ele-
ments of pain and dysfunction, but agreement
on specifics beyond that is hard to find.
Epidemiologic studies of TMD have meas-
ured various signs and symptoms in various
population groups, so summation of the state
of knowledge is difficult. Commonly measured
signs and symptoms include pain in the joint or
masseter muscles with joint movement; limita-
tions in mandibular movement; mandibular
deviations on opening; and joint clicking or
crepitus. Studies have used both self-report
questionnaires and clinical examinations to
obtain information. Many of what are referred
to as epidemiologic studies in fact are clinical
studies of patients receiving treatment, and thus
their results must be interpreted cautiously.
With regard to patients, there are three times as
many women TMD patients as men patients,
although no one knows why.29
There is general agreement that the preva-
lence of the commonly measured conditions
just listed is quite high, even among people
who do not perceive that they have a problem
requiring treatment.15,54,62,66,73,90 One study of
a representative population in Toronto found
that some 49% of adults responded positively
to one or more of nine questions regarding
symptoms, although a need for treatment was
found in only 3%-10%, depending on the case
23 Oral Cancer and Other Oral Conditions 301
definition used.46 However, it is very difficult to
interpret what these data mean, for it is com-
mon to find prevalent symptoms that have no
clinical significance.54,68 Is a clicking joint, for
example, a sign of impending trouble or is it of
no consequence? A 20-year longitudinal study
found that symptoms come and go over time
but that progression to severe pain and dysfunc-
tion is rare.49 Other longitudinal studies have
obtained similar results.17,48 It has been noted
that signs and symptoms are as common in
children and adolescents as they are in adults54
and are even reported in preschool children,92
although again the proper interpretation of
these findings is unclear. Clicking joints in ado-
lescents have been related to growth stages and
come and go in response to “natural longitudi-
nal fluctuations.”90 Cross-sectional studies can
therefore give misleading information on
prevalence and correlations.40
Although a great deal of TMD seems to have
been treated by the use of orthodontic appli-
ances, the current view is that occlusal discrep-
ancies such as attrition and premature contacts
are not a factor in TMD.10,30,74 Moreover, there
is no evidence that orthodontic treatment
increases the risk of TMD.39,43 It is widely
thought that TMD should be treated as a med-
ical orthopedic problem rather than a purely
dental one.13,22
The need for a multidisciplinary approach to
treatment is given weight by psychological stud-
ies of TMD patients. Such studies are essential
in addressing the question of whether TMD is a
discrete entity or whether it is part of broader
psychological disturbances. Clinical depression
is related to TMD.78 Profiles of TMD patients
have found that they tend to be of lower socio-
economic status,6 that they tend to report their
general health to be poorer than do nonpa-
tients,6,29,50 and that emotional distress and
feelings of lack of control over their lives are
common.6 (The cause-and-effect relationship is
not necessarily that emotional distress leads to
TMD. On the contrary, it is entirely likely that
the sequence is the other way around: continu-
ing TMD, with lack of relief from treatment,
could lead to emotional distress in an otherwise
normal person.) Patients with complex orofa-
cial pain conditions often do not respond as
expected to dental care.70 The state of the art
with regard to psychological correlates of TMD
302 The Distribution of Oral Diseases and Conditions
is confused, and the results of a number of stud-
ies have been contradictory.55,56,71
Research into this highly distressing condition
clearly has a long way to go before treatments
with a firm scientific base, let alone prevention
strategies, can be formulated. What is clear from
the research to date is that the condition is highly
complex and that multidisciplinary effort is
required for its better comprehension.
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 24 Fluoride: Human Health and Caries
Prevention
A CLASSIC EPIDEMIOLOGIC STUDY
ENVIRONMENTAL FLUORIDE
SOURCES AND AMOUNTS OF FLUORIDE
INTAKE
FLUORIDE PHYSIOLOGY
Absorption, Retention, and Excretion
Optimum Fluoride Intake
FLUORIDE AND HUMAN HEALTH
Early Studies
Mortality
Cancer
Down Syndrome
It is hard for today’s students to visualize what
caries used to look like in prefluoride days.
Periapical abscesses and gaping anterior lesions
were common, extractions of first molars in
young children were routine, and full extrac-
tions and complete dentures were virtually the
norm for older people. Although higher educa-
tional levels, better technology, and the spread
of middle-class standards have led to improve-
ment of this situation, fluoride ranks as a pri-
mary influence in better oral health because its
impact changed the way people thought about
dental health. It demonstrated to patients and
nonpatients alike that caries and subsequent
tooth loss were not inevitable. Just as impor-
tant, it helped dentists to reshape their attitudes
toward tooth conservation.
This chapter deals with the issues of how flu-
oride’s caries-inhibitory potential was first dis-
covered, how the human body physiologically
deals with fluoride when the material is
ingested, how fluoride affects our health, and
how it works to prevent caries. In this and subse-
quent chapters, we abbreviate the word fluoride
to its chemical symbol F to make reading easier.
It all begins with one of the great epidemiologic
studies in the history of health research.
Bone Density, Fracture Experience, and
Osteoporosis
Child Development
FLUORIDE TOXICITY
DENTAL FLUOROSIS
FLUORIDE AND CARIES CONTROL:
MECHANISMS OF ACTION
Fluoride and Plaque
Fluoride and Enamel
Fluoride and Saliva
Effects on Different Tooth Surfaces
EFFECTIVE USE OF FLUORIDE
A CLASSIC EPIDEMIOLOGIC STUDY
Dr. Frederick McKay, as a new dental graduate in
the early 1900s, headed west and opened a prac-
tice in Colorado Springs, Colorado. He soon
noticed that many of his patients had a curious
blotching of the enamel that he had not
encountered before. People in the area called it
“Colorado brown stain,” and to them it was just
a local oddity. It seemed harmless enough,
though it was disfiguring in some cases. McKay
was clearly a born scientist; he had an inquiring
mind and fine powers of observation, and
Colorado brown stain piqued his curiosity. In
1908 he began to investigate the extent of
Colorado brown stain in the surrounding area.
In his travels over the next few years, McKay
found that the condition was highly prevalent
in the Colorado Springs area. It was found only
in long-term residents, individuals who had
been born there or who had come to the area as
babies. Because the stain was difficult to polish
off, McKay reasoned that it must be caused by
an environmental agent that was active during
the period of enamel formation. To ensure that
his findings attracted some attention, McKay
was shrewd enough to enlist the collaboration
307
308 Prevention of Oral Diseases in Public Health
of G. V. Black, a major figure in dental history,
in writing the first description of what then
came to be called mottled enamel.15 This detailed
report, in the elegant prose of the time, is a trib-
ute to McKay’s investigative thoroughness.
McKay found that mottled enamel was
endemic in many other communities along the
Continental Divide and the plains to the east. It
was most prevalent where deep artesian wells
were the source of drinking water, and within
any community the persons affected had almost
invariably been users of the same water supply.
By the 1920s McKay had reached the conclusion
that the etiologic agent had to be a constituent
of some community water supplies, despite the
fact that chemical analyses all failed to identify
likely constituents. In communities such as
Andover and Britton, South Dakota, where he
found severe mottling, he advised mothers to
obtain their children’s drinking water from
sources other than the community supply. In
Oakley, Idaho, McKay found that children liv-
ing on the outskirts of the city, using water from
a private spring, were free of mottling. He
advised the citizens of Oakley to abandon their
old supply and tap this spring for a new source,
which the community did in 1925. McKay was
right, for children born in Oakley subsequent to
the change were free of mottled enamel.128
By 1930 new methods of spectro-
graphic analysis of water had been developed.
In 1931 McKay sent several samples of sus-
pected water to an Alcoa Company chemist
named Churchill, who was using these new
methods. Churchill identified F in each of the
samples, in amounts ranging up to 14 parts per
million (ppm).26 At around the same time, sim-
ilar findings were reported by investigators at
the University of Arizona161 and by a veterinary
group in Morocco, then still a French colony,
that was studying le darmous, the local name
given to an extreme degree of mottled enamel
found in Moroccan sheep.174
The immediate reaction of the scientific com-
munity to the identification of F in drinking
water was one of concern, because F in high
concentrations was known to be a protoplasmic
poison. The discovery led to the appointment in
1931 of the first dentist to the newly established
National Institute of Health. This was H.
Trendley Dean, who was transferred from else-
where in the U.S. Public Health Service to
become the one-person Dental Hygiene Unit,
an odd name for a unit formed to investigate
mottled enamel (it subsequently became the
National Institute of Dental Research in 1948).
Amidst this flurry of concern, however,
McKay had also noted some benefits that
seemed to accompany mottled enamel. In
1928, 3 years before F was identified in drinking
water, he was confident enough to publish his
view that caries experience was reduced by the
same waters that produced mottled enamel.127
A similar observation was made shortly after-
ward in England by Ainsworth,2 who like
McKay was an observant dentist with an inquir-
ing mind. Although McKay was not the first to
make this suggestion, none of the earlier
observers took the idea any further. McKay, and
Dean as well, are good examples of history’s
putting the right people in the right place at the
right time.
The task of defining the relationship of F to
mottled enamel now passed to Dean. His first
job was to map out the prevalence of mottled
enamel in the United States. Dean began like an
investigative reporter, writing extensively to
dental societies all around the country to ask for
their experiences. He received a good response
and published his first map on the distribution
of mottled enamel in 1933.32 His next step was
to develop a seven-point ordinal-scale index to
classify the full range of mottled enamel he had
seen, from the finest of lacy markings to the
stained and highly friable enamel seen with
extreme hypomineralization.33
Dean began using the term fluorosis to replace
mottled enamel in the mid-1930s.39 He patiently
surveyed children in many parts of the country,
using his original fluorosis index, and built up a
substantial body of information (what today we
would call a database) for analysis. He devised his
Community Fluorosis index based on his original
seven grades of severity.38 Studies through the
mid-1930s analyzed many drinking water sam-
ples for minerals and other chemical constituents,
but none apart from F could be related to fluoro-
sis.39,41 Dean chose his words carefully to define a
desirable F concentration as follows:
For public health purposes, we have arbitrarily defined the
minimal threshold of fluoride concentration in a domestic
water supply as the highest concentration of fluoride inca-
pable of producing a definite degree of mottled enamel in as
much as 10 percent of the group examined.39
 24
By the mid-1930s, Dean had concluded that
this “minimal threshold” level was 1 ppm F,34
and that fluorosis seen in communities with
water below 1 ppm F was “of no public health
significance.” 40 Soon afterward he defined
1 ppm F as “the permissible maximum.”45
Later in that decade of the Great Depression,
Dean condensed his original 1934 fluorosis
index to one using a six-point ordinal scale
(see Chapter 17) by combining the categories
of “moderately severe” and “severe.”42 He then
added numerical values to the categories to
permit quantitative comparisons among pop-
ulations. By 1942 Dean had documented the
prevalence of fluorosis for most of the United
States.36
Although he still documented fluorosis in
his studies, the main theme of Dean’s research
from then on was the F-caries relationship. In
the mid-1930s Dean matched his fluorosis data
for children in parts of South Dakota,
Colorado, and Wisconsin with the caries data
from an earlier 26-state survey in what today
would be called an ecologic study (see Chapter
13). Although he could hardly have failed to
notice the low caries experience in communities
with F-bearing water during his early surveys,
this was his first report in which he commented
on the inverse relationship between fluorosis
and caries.35
Encouraged by these preliminary data, Dean
chose four cities in central Illinois as study sites
in which to test the hypothesis that consump-
tion of F-containing water was associated with a
reduced prevalence of caries. Galesburg and
Monmouth, where Dean had already studied
fluorosis,40 used water from deep wells that
averaged 1.8 and 1.7 ppm F. Macomb and
Quincy used surface water averaging 0.2 ppm F.
Clinical examinations of children ages 12-14
years, all with lifetime residence in their respec-
tive cities, showed that more than twice as many
children in Galesburg and Monmouth were free
of detectable caries than in the two cities with
low-F water, and the mean number of perma-
nent teeth affected by caries in Galesburg and
Monmouth was half of that in the two cities
with low-F water.44 The evidence to support the
F-caries hypothesis was now stronger.
Although caries prevalence and severity were
low in Galesburg and Monmouth, fluorosis was
an obvious problem in both communities.
Fluoride: Human Health and Caries Prevention 309
Dean and the other investigators put it this way,
in the flowing prose of the time:
[It is] obvious that whatever effect the waters with relatively
high fluoride content (over 2.0 ppm of F) have on dental caries
is largely one of academic interest; the resultant permanent
disfigurement of many of the users far outweighs any advan-
tage that might accrue from the standpoint of partial control
of dental caries. On the other hand, the demonstration of such
marked dental caries differences as were observed at
Galesburg and Quincy made advisable a quantitative study of
the influence on dental caries of waters with lower ranges of
fluoride concentration. If marked inhibitory influences were
operative at concentration levels as low as the minimal
threshold of endemic fluorosis (1.0 ppm), the findings would
be of considerable import.43
The next logical step was therefore to define
the lowest F level at which caries was clearly
inhibited. This was done through a series of
investigations that have become known collec-
tively as the 21 cities study and that are rightly
considered a landmark in dental research. The
first part consisted of the results of clinical
examinations of children ages 12-14 with life-
time residence in eight suburban Chicago com-
munities with various but stable mean F levels
in their domestic water.43 The project was later
expanded by adding data from 13 addi-
tional cities in Illinois, Colorado, Ohio, and
Indiana.37 The collective findings of the 21 cities
study are depicted graphically in Figs. 24-1 and
24-2. Fig. 24-1 shows that dental caries experi-
ence in different communities dropped sharply
as F concentration rose toward 1 ppm, then lev-
eled off. Fig. 24-2 shows the dental fluorosis
experience that Dean found among the 12- to
14-year-olds in the 21 cities. Dean’s practice was
to show questionable fluorosis separately in his
reports, as we have done in Fig. 24-2. The data
in Fig. 24-2 suggest that, had “questionable”
fluorosis been included in the prevalence fig-
ures, then the level for “acceptable” fluorosis
might have been set at concentrations lower
than 1 ppm F.
Because the 21 cities study had a cross-sec-
tional design, the results confirmed the associa-
tion but could not by themselves establish the
cause-and-effect relationship between fluori-
dated water and reduced caries prevalence. But
the data in Figs. 24-1 and 24-2 did lead to the
adoption of 1.0-1.2 ppm as the appropriate con-
centration of F in drinking water in temperate
climates, a standard that remains in place today
310 Prevention of Oral Diseases in Public Health

12

10

8
Mean DMFT

0
0 0 0 0.1 0.1 0.1 0.1 0.2 0.2 0.3 0.4 0.5 0.7 0.9 1.2 1.2 1.2 1.3 1.8 1.9 2.6

Water fluoride concentrations (ppm F)

Fig. 24-1 Decayed, missing, and filled permanent teeth (DMFT) in children ages 12-14 in 21 cities in the late
1930s, related to the fluoride concentration.37,43

100
Questionable
Mild/very mild
80
Moderate/severe

60
Percent

40

20

0
0 0 0 0.1 0.1 0.1 0.1 0.2 0.2 0.3 0.4 0.5 0.7 0.9 1.2 1.2 1.2 1.3 1.8 1.9 2.6

Water fluoride concentrations (ppm F)

Fig. 24-2 Fluorosis experience of children ages 12-14 in 21 cities in the late 1930s, related to the fluoride
concentration of drinking water.37,43
 24
in the United States. These results also set the
stage for a prospective test of the F-caries
hypothesis, first suggested in 1943.8 The years of
study of people using water with F levels much
higher than the proposed 1 ppm (detailed later
in this chapter) were sufficient to convince pub-
lic authorities that the prospective tests could be
carried out in safety. These first prospective stud-
ies are described in Chapter 25.
Trendley Dean died in 1962. Those who
knew him said that he could be autocratic, and
the reverence he inspired in his colleagues may
too often have been expressed as uncritical
acceptance of all he did. But Dean had the
researcher’s virtues of dogged perseverance and
remorseless logic as he progressed from one
stage to the next. His grasp of the concept of
“databasing” and his analytic mind make us
wonder what he could have done with modern
computer technology. Although knowledge of
F’s effects has advanced considerably since those
days, we enjoy the benefits of F today because of
the pioneering research of Dean and his col-
leagues. In time, it led to the substantial decline
in dental caries in high-income nations, one of
history’s major public health success stories.
ENVIRONMENTAL FLUORIDE
Fluorine is one of the most reactive elements
and therefore is never found naturally in its ele-
mental form. The F ion, however, is abundant in
nature and occurs almost universally in soils
and waters in varying, but generally low, con-
centrations. Seawater contains 1.2-1.4 ppm F.181
Fresh surface water generally has very low con-
centrations, 0.2 ppm F or less, whereas concen-
trations of up to 29.5 ppm F have been recorded
in deep well water in Arizona120 and concentra-
tions of over 40 ppm in boreholes in Kenya.112
F’s ubiquity in soil and water means that all
plants and animals contain F to some extent.
Given this environmental omnipresence, it
seems likely that all forms of life have evolved
to thrive with continuous exposure to small
amounts of F.
SOURCES AND AMOUNTS
OF FLUORIDE INTAKE
Humans absorb F from air, food, and water.
F intake from air is usually negligible, around
Fluoride: Human Health and Caries Prevention 311
0.04 mg F/day.180 Exceptions can occur around
some industrial plants that work with F-rich
material, such as aluminum smelters with inad-
equate safeguards to prevent the escape of
F-containing compounds. Such environmental
hazards should be controlled to the extent pos-
sible, an issue that has nothing whatever to do
with the use of F to control caries.
F’s abundance in soils and plants means that
everyone consumes it to some extent. Studies to
estimate the average daily intake of F from all
sources have provided fairly consistent results,
despite both the variability of the human diet
and methodologic difficulties inherent in ana-
lyzing such minute amounts. Estimates for an
adult North American male in an area with fluor-
idated water fall within the range of 1-3 mg F/day
from food and beverages,30,60,102,141,159,160,165
decreasing to 1 mg F/day or less in an area with-
out fluoridation.30,102,141,159,160 “Market basket”
analyses indicated that 6-month-old infants
ingested 0.21-0.54 mg F/day in four American
cities with different F concentrations in the
drinking water. For 2-year-olds in the same cities,
the range was 0.41-0.61 mg F/day.139,140
F ingestion in infancy is a matter of some
concern because of the risk of dental fluorosis.
Methodical estimates of F intake by infants have
come from the Iowa F studies, initiated in
the 1990s, which showed that F exposure
among infants is extensive and variable. The
Iowa studies documented the F exposures of
newborn infants at periodic intervals through
extensive interviews about F exposure from
drinking water, toothpaste, and dietary supple-
ments. During the first 3 years of life, F inges-
tion from these sources averaged 0.37-0.45 mg
daily from birth to 3 months, 0.5 mg at 6-9
months, 0.36 mg at 12 and 16 months, and
0.5-0.63 mg from 16 to 36 months.107 Although
mean intakes in Iowa were similar to those esti-
mated in the earlier market basket surveys, there
was a considerable range of intakes, with 90th
percentile values well above the means and
medians. When values were expressed as F
intake per kilogram of body weight, nearly half
of the children up to 6 months of age were
found to be exceeding the desirable limits,
although this proportion dropped considerably
at later ages. The upper limit of intake for 12-
month-old children, beyond which fluorosis
risk is greatly increased, has been estimated at
312 Prevention of Oral Diseases in Public Health

0.43 mg F/day.20 The 12-month-old children in

the Iowa studies averaged 0.36 mg F/day,107 but
more than 25% of them were ingesting F above
that upper limit.
The principal overall finding of the Iowa
studies is the great variability of F intake during
infancy, which is to be expected given the range
of dietary choices for infants and the range of
F concentrations in drinking waters. Despite the
difficulty in conducting studies like these, the
results are similar to those found in the market
basket surveys described earlier and in studies
from other countries.70,115
For most people, water and other beverages
provide some 75% of F intake, whether or not
the drinking water is fluoridated.160 This may
occur because many soft drinks and fruit
juices are processed in cities with fluoridated
water, or it may reflect variable F content of
the ingredients. One brand of grape juice in
North Carolina, for example, was found to
contain more than 1.6 ppm F, even when
reconstituted with deionized water.143 Even in
soft drinks of the same brand, F levels can vary
considerably due to production at different
sites. 76 Another source of high F intake for
infants is powdered infant formula reconsti-
tuted with fluoridated drinking water.22 The F
content of some tested beverages is shown in
Table 24-1.
FLUORIDE PHYSIOLOGY
Although the use of F is a contribution to the
public’s health of which dentistry can be proud,
F compounds must be handled responsibly and
with respect. Everyone in dentistry should
understand how the human body handles
ingested F so that the material can be used safely
and efficiently.
Absorption, Retention, and Excretion
Ingested F is absorbed mainly from the upper
gastrointestinal tract, and some 95% of ingested
F is absorbed. Absorbed F is transported in the
plasma and is either excreted or deposited in
the calcified tissues. Most absorbed F is excreted
in the urine; a single ingestion of 5 mg F by an
adult is absorbed and cleared from the blood in
8-9 hours.180 F ingested on an empty stomach
produces a peak plasma level within 30 min-
utes. The time of the plasma peak is extended,
and the level of the peak reduced, if the F is
taken with food. This is probably because of the
binding of some F with calcium and other diva-
lent and trivalent cations. When F absorption is
inhibited in this way, fecal excretion of F
increases.50
Studies of what is called the body burden of F,
meaning the amount that can be safely
absorbed and the point at which F absorption

Table 24-1 Fluoride concentration (in ppm) of various beverages available in a nonfluoridated and a fluoridated
community in Alberta, Canada, and in various communities in North Carolina and Iowa28,96,143
Beverage Nonfluoridated, Canada Fluoridated, Canada North Carolina* Iowa

Drinking water 0.23 1.08 — —

Milk† 0.03 0.03 — —
Juice (commercially prepared)‡ 0.80 0.80 0.36 0.56
Juice (home reconstituted) 0.21 1.06 — —
Apple-grape juice (commercially — — — 0.64
prepared)
Carbonated drinks‡ 0.80 0.80 0.74 —
Gatorade — — 0.85 —
Soup 0.21 1.06 — —
Tea 1.33 2.18 2.56 1.41
Coffee 0.23 1.08 — —
*Means of samples from six cities.
†Available fluoride.
‡Commercially available prepared juice and the carbonated drinks in Canada both came from a fluoridated large city; for Iowa the figure is

the mean for 532 juices.

 24
become a health concern, have relied mostly on
urinary volumes and plasma concentrations as
the primary measures. Samples of both are rela-
tively simple to obtain, although both measures
reflect only recent F intake (i.e., during the pre-
vious 3-4 weeks) rather than lifetime intakes.
Urinary concentrations can vary considerably
with fluid intake during the period of F expo-
sure,49 and a 24-hour sample is required for
accuracy. Accurate monitoring of plasma levels
in individuals also requires frequent measure-
ment because of normal hour-to-hour fluctua-
tions. Plasma F concentrations are more closely
correlated with urinary flow rates than with uri-
nary F concentrations.51 Although there is no
absolute measure of lifetime F intake, even the-
oretically, the closest measure of long-term F
intake would be based on bone F content.
However, for research purposes, this is a theo-
retical concept only; people do not volunteer to
give bone samples!
F balance is the net result from the accumu-
lated effects of F ingestion, degree of F deposi-
tion in bones and teeth, mobilization rate of
F from bone, and efficiency of the kidneys in
clearing absorbed F.
Plasma F is found in ionic and nonionic
forms. The biologic significance of the non-
ionic form has not yet been determined, and its
concentration is independent of F intake.
Absorbed F is transported by plasma as ionic F.
It is the level of this ionic F that rises temporar-
ily after F ingestion and then drops rapidly;
ionic F levels are not homeostatically regulated.
In a healthy adult male living in an area with
fluoridated water, plasma F levels are around
0.019 ppm (1 μmol/L), although this level fluc-
tuates throughout the day.50 Plasma levels are
generally higher in persons living in fluoridated
communities than in those living in nonfluori-
dated communities. Plasma F levels in persons
with chronic kidney failure can rise to 0.05-0.09
ppm F (2.6-4.7 μmol/L) without affecting
health.90 Nephrotoxic plasma F values in
healthy individuals have been estimated at
0.95 ppm F (50 μmol/L).
F has an affinity for calcified tissues, that is,
bone and developing teeth. F that is not
excreted is deposited in these hard tissues,
although storage is dynamic rather than inert.
Bone F levels (from postmortem assays) range
from 800 to 10,000 ppm, depending on many
Fluoride: Human Health and Caries Prevention 313
factors, including age and F intake. F levels in
the outer few microns of dental enamel range
from 400 to 3000 ppm and decrease rapidly
with greater enamel depth. F concentrations in
soft tissue rise or fall in parallel with plasma F
levels, but because healthy excretion and depo-
sition mechanisms operate so rapidly, there is
negligible retention of F in the fluids of soft tis-
sues other than the kidney.180 Some F has been
found in the aorta, associated with calcification
of that blood vessel. Deposition in the placenta
is also associated with islets of calcified tissue.55
A greater proportion of ingested F is excreted in
older persons than in the young because the
growing skeleton in young people absorbs
more F175,182 and probably because children
have lower renal clearance rates than adults.164
Because of the importance of the kidneys in
maintaining F balance, the only disease condi-
tion that requires medical consideration with
regard to F ingestion is chronic kidney failure.
Patients who receive renal dialysis for long peri-
ods with F-free water have maintained plasma
levels of 0.06 ppm F, whereas in some inadver-
tently receiving dialysis with fluoridated water
(definitely not a recommended procedure) lev-
els as high as 0.24 ppm F have been recorded.
Although a plasma level of around 0.09 ppm
F had been suggested as the upper limit before a
kidney patient undergoing dialysis should
reduce F intake, evidence for this recommenda-
tion has come from only a few case studies.90
With today’s standards for dialysate fluid, cur-
rent medical opinion is that even persons with
severe renal impairment can consume fluori-
dated water without ill effects as long as they are
receiving regular dialysis treatment.
Aluminum, iron, and other minerals create
greater technical problems for the renal dialy-
sis process than does F. The standard for
dialysate water set by the Association for the
Advancement of Medical Instrumentation is
that the F content should not exceed 0.2 ppm.94
Water used in renal dialysis should first be
treated by reverse osmosis, which is superior
to the older process of deionization in that
it removes F and other minerals almost
entirely.166
Optimal Fluoride Intake
Frank McClure, a biochemist with the U.S.
Public Health Service, estimated in 1943 that the
314 Prevention of Oral Diseases in Public Health
“average daily diet” contained 1.0-1.5 mg F, or
about 0.05 mg F/kg body weight per day in chil-
dren up to 12 years of age.118 McClure’s estimate
somehow came to be interpreted as the lower
limit of the range of “optimal” F intake. A widely
quoted 1974 report56 suggested that 0.06 mg
F/kg body weight per day was optimal, although
this estimate was based only on a number of
personal opinions. The intake range of 0.05-0.07
mg F/kg body weight per day was suggested as
optimal in 1980139; this is equivalent to 3.5-4.9
mg F/day for a 70-kg (154-lb) man. For a 10-kg
infant (22 lb; i.e., a 12- to 18-month-old child),
this optimal intake is equivalent to 0.45-0.64
mg F/day. (By comparison, in the Iowa studies
described earlier, the 90th percentile of daily F
ingestion for 16-month-old children was found
to be 0.775 mg.)
The National Research Council, the body
that establishes recommended dietary
allowances for the United States, classified F as a
“beneficial element for humans” because of its
positive impact on dental health.134 The coun-
cil at one time considered F an essential nutri-
ent,133 but it backed away from that position
because an essential role for F in human growth
studies could not be confirmed and because the
physiologic mechanism by which F would
influence growth was unknown. Available evi-
dence did not justify classifying F as an essential
element by accepted standards.134 Nutritional
requirements became recorded as dietary refer-
ence intakes in the late 1990s, with an “adequate
intake” level for F set at 0.01 mg/day for chil-
dren 0-6 months. For all ages above 6 months
the adequate intake was set at 0.05 mg F/kg/day,
so the absolute intake amount increases with
increasing weight to a maximum for adults age
19 or older of 4 mg/day for males and 3 mg/day
for females.85,86 It was not clear on what these
intake levels were based.
The discussions about “optimal” intake are
vague about what this intake is optimal for.
The implication is that this degree of ingestion
is optimal for caries resistance, but as will be
described later in this chapter, ingested F plays
only a minor role in caries control relative to
intra-oral F. It is also worth noting that
McClure’s 1943 comment was observational,
although it somehow was turned into a recom-
mendation over time. Empirical evidence sug-
gests that F intake of 0.05-0.07 mg/F/kg/day in
childhood is a broad upper limit if unesthetic
fluorosis is to be avoided.20 There is no evi-
dence to link this range of F ingestion with
caries inhibition, so we suggest that the term
optimal intake be dropped from common
usage.
FLUORIDE AND HUMAN HEALTH
Early Studies
Quite a lot was known about F at the time of
Dean’s appointment to the NIH Hygiene Unit
in 1933, 117 but details of a safe range of F
intake for humans were sketchy. The first study
relating bone fracture experience to the F con-
centration in home water supplies (a subject
revisited in the 1990s) concluded that there
was no relationship.119 McClure then demon-
strated the close relationship between urinary
F concentrations and the F levels of domestic
water.121 His balance studies during World War
II, in which young men lived in rooms main-
tained at varying temperatures and humidity
levels and received varying amounts of F in
food and water, led to the conclusion that the
elimination of absorbed F via urine and per-
spiration is almost complete when the quan-
tity absorbed does not exceed 4-5 mg daily.125
McClure suggested that this may be the limit of
F that could be ingested without “appreciable
hazard” of excessive F storage in the body.
Higher F intakes were likely in communities
such as Bartlett, Texas, however, where commu-
nity water carried about 8 ppm F. A long-term
study of the residents of Bartlett, conducted by
a U.S. Public Health Service team, began in
1943. Apart from severe dental fluorosis, the
study found no adverse effects of long-term
ingestion of this high-F water,105 although
postmortem bone F concentrations were high.
Numerous animal studies in the early years
of water fluoridation104,109,116,122,124,186-188
supported the results from studies in human
populations.
Although not every possible hypothesis
regarding F and human health was tested prior
to initiation of controlled fluoridation, there
was sufficient research evidence to provide rea-
sonable assurance that controlled fluoridation,
with up to 1.2 ppm F in the drinking water,
could be instituted in North America without
creating any public health hazard.
 24
Mortality
For the United States as a whole, no differences
could be found in 1949-50 death rates between
32 cities with 0.7 ppm F or more and 32 ran-
domly selected nearby cities with 0.25 ppm F or
less in the drinking water. Mortality rates were
similar for cancer, heart disease, intracranial
lesions, nephritis, and cirrhosis of the liver.71 In
1979 mortality rates for 478 cities with popula-
tions of 25,000 or more were examined for the
periods 1949-50, 1959-61, and 1969-71. Data
were collected on total deaths as well as those
attributed to cardiovascular disease, renal con-
ditions, and cancer. No differences between
fluoridated and nonfluoridated communities
were found.157
Cancer
The 1979 mortality study157 was conducted as a
response to testimony before a congressional
committee in 1975 by Burk and Yiamouyiannis
that fluoridation led to an increase in cancer
deaths.19 Their argument was based on a com-
parison of mortality data for the 10 largest fluor-
idated American cities between 1950 and 1970
and mortality data for 10 selected nonfluori-
dated cities over the same period. The crude
mortality data, unadjusted for age, sex, or race,
showed a greater increase in cancer deaths in
the fluoridated cities over the 20-year period.
Criticism of this analysis was based on the inap-
propriateness of using crude mortality data,
because the populations of the big cities during
that 20-year period had become older and
poorer, and had changed their ethnic composi-
tion. Yiamouyiannis and Burk repeated their
work in 1977, this time with some age adjust-
ment,185 and claimed that their data still
showed an excess of cancer deaths in the fluori-
dated cities. But a number of independent
analyses of the same data were conducted in
both Britain and the United States and
employed more detailed age-sex-race adjust-
ments; none could find a link between cancer
incidence and consumption of fluoridated
water.47,52,82,137,149,167
One result of the Burk-Yiamouyiannis testi-
mony was that a congressional committee
directed the National Cancer Institute to carry
out animal studies on the potential carcino-
genicity of F. The National Toxicology Program
(NTP) was responsible for conducting these
Fluoride: Human Health and Caries Prevention 315
studies, which were performed with several ani-
mal species and used four concentration of F in
the drinking water: 0, 11, 45, and 79 ppm F. (Use
of extremely high levels of the test material is
standard practice in toxicology studies to avoid
having to use huge populations of animals.) The
studies, which tested the effects of the water on
the animals over 2 years, took longer than
expected, but the NTP finally issued an extensive
draft report in 1990. Although a number of dif-
ferent cancers occurred in both test and control
animals, the report found “equivocal evidence”
of an excess incidence of osteosarcoma, a rare
form of bone cancer, in male rats of a particular
strain.171 Three of the four osteosarcomas were
in the rats ingesting 79 ppm F; the fourth was at
45 ppm F. Subsequent review of the data by stat-
isticians, as well as a public hearing and consid-
erable media attention, did not change this
gray-zone conclusion.
In response, the Assistant Secretary for Health
incorporated the NTP findings into a broader
review of F and the environment, conducted by
a special committee appointed by the U.S.
Public Health Service. This committee reached
the following conclusion on cancer risk:
Optimal fluoridation of drinking water does not pose a
detectable cancer risk to humans as evidenced by extensive
human epidemiological data available to date, including the
new studies prepared for this report. While the presence of
fluoride in sources other than drinking water reduces the abil-
ity to discriminate between exposure in fluoridated as com-
pared to non-fluoridated communities, no trends in cancer
risk, including the risk of osteosarcoma, were attributed to the
introduction of fluoride into drinking water in these new stud-
ies. During two time periods, 1973-1980 and 1981-1987,
there was an unexplained increase of osteosarcoma in males
under age 20. The reason for this increase remains to be clar-
ified, but an extensive analysis reveals that it is unrelated to
the introduction and duration of fluoridation.172
The NTP report raised some interesting issues
about risk assessment in the modern environ-
ment. Bone cancer is not common: of the
538,000 estimated cancer deaths in the United
States in 1994, some 1075 (0.19%) were bone
cancers of all kinds.16 Case-control studies pres-
ent the difficulty of documenting precisely all F
exposure during a person’s lifetime, which
biases the results of such studies toward the
null hypothesis (i.e., imprecise data make
it more likely that the null hypothesis cannot
be rejected). Risk assessment studies can be
316 Prevention of Oral Diseases in Public Health
conducted with animals, but the question
always remains: what is the relevance of health
effects in rats drinking water with 79 ppm F to
humans drinking water with 1-4 ppm F? The
marginal nature of the findings makes answer-
ing the question even more difficult. In addi-
tion, a large number of tests were conducted in
the NTP studies, and statistical logic tells us that
false results will occur about five times in each
100 tests (see Chapter 13). In epidemiologic
research involving humans, neither ecologic
studies63,130 nor case-control studies64,126 have
found any association between osteosarcoma
and previous F exposure.
Down Syndrome
A claim that water fluoridation caused an
increase in the congenital malformation known
as Down syndrome was put forward in a series
of papers in the mid-1950s.145-147 The studies
claimed to show from birth records in
Wisconsin and Illinois that the incidence of
Down syndrome was higher in fluoridated than
in nonfluoridated areas, but there were errors in
the research design.153 The most serious error
was the assumption that the city of birth was the
place of residence of the mother, which is
clearly not the case for hospitals serving a large
rural population. More rigorous independent
studies in the United States and Britain have
subsequently failed to show any correlation
between fluoridation and Down syn-
drome.14,53,54,135 A systematic review in 2001
reached the same conclusion.184
Bone Density, Fracture Experience,
and Osteoporosis
Bone fragility conditions (e.g., preventing spon-
taneous vertebral fracture in the elderly as a
result of osteoporosis) have been treated for
years with high doses of F combined with cal-
cium, estrogen, and vitamin D. Controlled clini-
cal trials have shown that high doses of F (30-60
mg/day), administered under medical supervi-
sion, can increase vertebral bone mass and
reduce the vertebral fracture rate.142 These favor-
able changes do not come without problems,
however, for the new bone can be imperfectly
mineralized, and a good proportion of patients
do not respond to treatment.74 Treatment also
seems ineffective in preventing further fractures
in patients who already have a fracture at first
presentation.99 The main concern is that the
positive effects seen in the vertebral column,
which is mostly cancellous bone, are not seen in
the appendicular skeleton, which is mostly cor-
tical bone. Indeed, fracture rates in the appen-
dicular skeleton have actually been shown to
increase with intensive F treatment.73,148
Although an international conference in 1988
recommended F treatment for vertebral crush
syndrome,74 high-dose F treatment (up to 80 mg
F/day) for bone fragility conditions is no longer
recommended in the United States,78,98 nor is F
therapy seen as a measure that can prevent frac-
tures resulting from osteoporosis.73,129
These studies answer one prominent ques-
tion about the health effects of F: they show that
even frail elderly people can tolerate large F
intakes (e.g., 30-60 mg F/day), vastly higher
than anyone would experience with fluoridated
drinking water. A more pertinent issue in den-
tistry is the effect of fluoridated water on bone
fragility or fracture experience. Day-to-day use
of fluoridated water obviously results in much
lower daily intakes (1-3 mg F/day for adults, see
earlier) than those seen at the therapeutic doses
just described.
In the research by McClure mentioned ear-
lier, McClure studied the relation between self-
reported bone fracture experience and exposure
to fluoridated water among young men during
World War II and reported no association. As in
other early studies,13,66 no account was taken of
confounding factors such as body mass, med-
ication use, and dietary factors, and the radi-
ographic techniques of that era have been
shown to be insensitive. In more recent times, a
series of ecologic studies (see Chapter 13) to
assess the risk of bone fracture in those drinking
fluoridated water have produced mixed results:
decreased risk,77,87,103,144,158 no associa-
tion,5,92,108,111,168 and increased risk.29,31,88,89
The extent of increased risk in the latter group of
studies was generally low, with relative risks in
the range of 1.08-1.41. Given the lack of preci-
sion that is part of ecologic studies, it is not sur-
prising that this body of research does not yield
clear conclusions for either increased risk or a
protective effect of F. Extensive reviews of the lit-
erature have also reached the conclusion that
no relationship can be discerned between bone
fracture experience and exposure to water with
1 ppm F.3,46,78,91,97,98
 24
Results of research in which data are col-
lected from individual study participants are
likely to have higher validity than results of eco-
logic studies. Studies conducted in several rural
Iowa communities found reduced radial bone
mass and slightly higher fracture experience in a
town where the drinking water contained 4.0
ppm F.162,163 However, a study of some 2000
women in western Pennsylvania found no asso-
ciation between long-term exposure to water
fluoridated at a lower level (1.0 ppm F) and
bone mineral density and fracture experience.24
A small Canadian study found only beneficial
effects on skeletal growth from growing up in a
fluoridated area.6
Research continues, but it can be stated that
the evidence supports only marginal benefits to
bone from fluoridated water, and there is
no evidence that bone fracture experience
is altered by exposure to drinking water con-
taining 1.0 ppm F.132
Child Development
An important study of the effect of F on children
was the Newburgh-Kingston fluoridation proj-
ect, one of the original fluoridation field trials,
which began in 1945. Participating children
received a complete physical examination,
selected physical measurements were taken, and
laboratory and radiographic studies were per-
formed. No significant differences in general
health or body processes between children in
the two cities were seen, and no radiographic
differences in bone density could be demon-
strated. There was essential similarity in vision
and hearing test results and in measures of
skeletal maturation, hemoglobin level, erythro-
cyte and leukocyte counts, and quantity of
sugar, albumin, red blood cells, and casts in
the urine. At the final examination, 19 of 476
children in fluoridated Newburgh (4.0%) and
20 of 405 children in non-fluoridated Kingston
(4.9%) were referred to their family physicians
for conditions including such minor ailments
as plantar wart or ringworm. Long-term down-
ward trends in stillbirths and maternal and
infant mortality rates continued in each of the
cities. The overall conclusion reached was that
no differences of medical significance could be
found between the two groups of children.156
As part of the main health study in the
Newburgh-Kingston fluoridation project, 100
Fluoride: Human Health and Caries Prevention 317
boys in each city, age 12 at final medical exami-
nation, were selected from the 881 participants
in both cities for a substudy of specific urinary
components.155 Children who had recently
been ill were excluded because results could
otherwise have been confounded by a variety of
unrelated conditions. No difference between
the two populations was found.
FLUORIDE TOXICITY
There is a world of difference (literally!)
between a single intake of 5.0 g F and constant
intake of 1-3 mg F daily. F is thus like many
other nutrients: beneficial in small amounts,
toxic in high amounts. This gradation in
response with variations in dose is a common
pharmaceutical phenomenon and is known as
a dose-response relationship.
Information on F toxicity levels cannot, of
course, be taken from controlled studies with
humans. Available data come from a mix of case
studies of various kinds and research on work-
ers in certain industrial processes. The classic
work in occupational F toxicity is that of the
Danish scientist Kaj Roholm, who studied cryo-
lite workers in aluminum plants during the
1930s. Their daily absorption was estimated at
0.2-1.0 mg F/kg body weight (about 14-68 mg
F/day for a 150-lb adult). Some workers had
been employed as long as 31 years. Under these
conditions a number of toxic effects were
observed, principally gastric complaints and
osteosclerosis.
Ingestion of a single dose of 5-10 g of NaF by
an adult male (32-64 mg F/kg body weight)
results in a rather unpleasant death in 2-4 hours
if first aid is not rendered immediately. From
that lower limit of 32 mg F/kg body weight,
the estimated equivalent dose for a 10-kg child
(12-18 months old) is 320 mg F.75 Crippling
skeletal fluorosis can eventually occur in an
adult with daily ingestion of 10-25 mg F over a
period of 10-20 years. The evidence on known
toxic effects of F ingestion is summarized in
Table 24-2.
If an individual is known or suspected to
have taken a potentially toxic amount of F, first
aid is to induce vomiting as quickly as possible
or to have the person ingest a material to bind F:
milk is usually the most readily available. The
American Dental Association recommends, as a
318 Prevention of Oral Diseases in Public Health
safety precaution, that F materials for home use
contain no more than 264 mg F if packaged in a
bulk container (tablets, mouthrinse) or up
to 300 mg F if the F material is individually
packaged.
At the other end of the toxicity spectrum,
there are many instances of remarkable tolera-
tion of high quantities of F without ill effects,
such as in osteoporosis patients as described
earlier. Adverse effects in these patients are
reported to be usually no worse than nausea,
stomach pains, pain in the extremities, and
occasional diarrhea. The greatly elevated levels
of plasma F may also be associated with some
arthritis-type joint pain, but it is not certain
whether this pain comes from the treatment or
the disease itself.
DENTAL FLUOROSIS
Dental fluorosis is a permanent hypomineral-
ization of enamel that is characterized by
greater surface and subsurface porosity than in
normal enamel and that results from exposure
of the developing tooth to excess F during matu-
rational stages.58 Its distribution and risk factors
are described in Chapter 22.
Table 24-2 Degrees of potentially toxic ingestion of fluoride
Effect
Acute fatal poisoning, adults79
Acute fatal poisoning, 10-kg child75
Acute fatal poisoning, 3-year-old child83
Acute fatal poisoning, adult renal dialysis patient61
Acute fatal poisoning, adult male65
Short-term nonserious nausea in elementary school
children81
Nausea and vomiting in adults176
Severe skeletal fluorosis79
Osteosclerosis, radiographic changes in human bone80
Dental fluorosis59
Acute fatal poisoning in animals79
Interference with reproduction, thyroid disturbance,
loss of body weight, and lameness in cattle79
*With drinking water fluoridated at 1 ppm, an adult would have to drink 660 gal in 2-4 hr to reach the lower limit of a fatal dose. A 10-kg
child (12-18 mo old) would have to drink 85 gal in 2-4 hr. Severe skeletal fluorosis could only result from drinking 2.6-6.6 gal of water
daily for 10-20 yr if none of the fluoride were excreted.
FLUORIDE AND CARIES CONTROL:
MECHANISMS OF ACTION
F works best to prevent caries when a constant,
low level of F is maintained in the oral cavity.27 Its
most important caries-inhibitory action is
posteruptive and takes place at the plaque-
enamel interface.57 The action of F in preventing
caries is multifactorial; its effect comes from a
combination of several mechanisms. Three major
mechanisms of action have been identified, sum-
marized in Box 24-1, although some possible
additional mechanisms have been hypothesized.
It has long been held that preeruptive expo-
sure to F inhibits caries to some degree. In this
“preeruptive” model, F is said to act by becom-
ing incorporated into the developing enamel
hydroxyapatite crystal and thus reducing
enamel solubility. It has been argued that
preeruptive benefits are especially important for
reducing pit-and-fissure lesions.69 This caries-
preventive action by F was assumed for many
years to be F’s primary effect, but the actual sup-
portive evidence is largely associative. Any
preeruptive effect on caries inhibition is likely
to be minor; the evidence for posteruptive F
action is much stronger.
Fluoride Intake and Time*
2.5-5.0 g, in 2-4 hr
320 mg, in 2-4 hr
Approximately 435 mg, in approximately 3 hr
Dialysate fluid 35-50 ppm F, for 3 hr
17.9 mg F/kg body weight, for 24 hr
93-375 ppm F in drinking water, small amounts;
symptoms within 30 minutes
Nausea with ingestion of an estimated 80 mg F over a
few hours, vomiting from ingestion of an estimated
143 mg F over a few hours
10-25 mg F daily, for 10-20 yr
8-20 mg F daily, for 10-20 yr
<0.1 mg F/kg body weight/day during tooth
development (i.e., the first 8 yr)
Approximately 50 mg F/kg body weight
40-60 ppm F in feed daily for several years
 24
BOX 24-1 Three Principal Mechanisms By Which
Fluoride Inhibits the Development of Dental Caries
Posteruptive
1. Promotion of remineralization and inhibition of
demineralization of early carious lesions.
2. Inhibition of glycolysis, the process by which
cariogenic bacteria metabolize fermentable
carbohydrates.
Preeruptive
3. Some reduction in enamel solubility in acid by
preeruptive incorporation of fluoride into the
hydroxyapatite crystal.
Fluoride and Plaque
The topical effect of a constant infusion of low-
concentration F into the oral cavity, such as
occurs with drinking fluoridated water or regu-
larly brushing with a F toothpaste, is to inhibit
demineralization and enhance remineraliza-
tion during the repeated cycles of demineraliza-
tion and remineralization (that awkward
phrase is often shortened to demin-remin) in the
early stages of the carious process. F introduced
into the mouth is partly taken up by dental
plaque, in which some 95% of it is held in
bound form rather than as ionic F. Plaque con-
tains 5-10 mg F/kg wet weight in low-F areas
and some 10-20 mg F/kg wet weight in fluori-
dated areas. The bound F can be released in
response to lowered pH,169 and F is taken up
more readily by demineralized enamel than by
sound enamel.179 The availability of plaque F to
respond to the acid challenge leads to the grad-
ual establishment of a well-crystallized and
more acid-resistant apatite in the enamel sur-
face during demin-remin.25,95,170 This means
that F can be incorporated into the enamel crys-
tal, but more through cycles of demin-remin
than through preeruptive absorption.
F in plaque also inhibits glycolysis, the
process through which fermentable carbohy-
drate is metabolized by cariogenic bacteria to
produce acid. F from drinking water and tooth-
paste concentrates in plaque, where its concen-
tration is governed by the concentration of
plaque calcium.183 Plaque contains higher lev-
els of F than does saliva.72,160 There is also some
evidence that plaque F can inhibit the produc-
Fluoride: Human Health and Caries Prevention 319
tion of extracellular polysaccharide by cario-
genic bacteria, a necessary process for plaque
adherence to smooth enamel surfaces.72
In addition to these mechanisms, high-
concentration F gels may have a specific bacteri-
cidal action on cariogenic bacteria in the
plaque. These gels also leave a temporary layer
of a material resembling CaF2 on the enamel
surface, which is available for release when the
pH drops at the enamel surface.136 At lower
concentrations, Streptococcus mutans has been
shown under laboratory conditions to become
less acidogenic through adaptation to an envi-
ronment in which F is constantly pres-
ent.17,18,114,151 It is not yet known whether this
ecologic adaptation reduces the cariogenicity of
acidogenic bacteria in humans.173
Fluoride and Enamel
In the early days of F research, it was assumed
that F’s inhibition of caries depended on its
preeruptive incorporation into developing den-
tal enamel, which thus reduced enamel solubil-
ity in demineralizing acids.38,123 In most of the
early fluoridation studies, greater caries reduc-
tions were found in children who were born
after fluoridation began than in those for whom
fluoridation began after birth.23,62,67,84,93 But it
was also clear that caries inhibition occurred in
teeth that had already erupted when fluorida-
tion began7,9,100,101,152 and in first molars that
were erupting when fluoridation began.10,12,154
It became evident to researchers as early as
the mid-1970s that a higher concentration of F
in enamel could not by itself explain the exten-
sive reductions in caries that F produced.106 At a
depth of 2 μm, enamel F concentrations aver-
aged around 1700 ppm in nonfluoridated areas
and 2200-3200 in areas fluoridated at 1 ppm.
Even in areas with 5-7 ppm F, enamel F concen-
trations rose only to 4800 ppm,1 which shows
that enamel F is poorly correlated with water F
levels. If the preeruptive hypothesis were true
(i.e., preeruptive F uptake by developing
enamel is the major factor in F’s cariostatic
effects), one would expect caries experience in a
population to be inversely related to enamel
F concentrations, but such is not the case.27
The converse also holds; that is, it has been
observed that higher concentrations of enamel
F do not necessarily mean than caries will not
occur.4 The theoretical concentration of F in
320 Prevention of Oral Diseases in Public Health
pure fluorapatite that would reduce its acid sol-
ubility is around 38,000 ppm,177 a concentra-
tion that is not even approached in human
dental enamel. So although some preeruptive
effect of F can be inferred from field stud-
ies,21,48 any such action is likely to be a minor
part of the overall impact of F.
The most revealing epidemiologic study on
the caries-inhibitory action of F came from the
Tiel-Culemborg fluoridation study in the
Netherlands,68 in which caries was recorded as
(1) incipient lesions confined to enamel, and
(2) dentinal lesions. Although, as would be
expected, there were considerably fewer denti-
nal lesions in fluoridated Tiel than in nonfluori-
dated Culemborg after 15 years of fluoridation,
there was no difference between the two com-
munities in lesions confined to enamel. This
finding means that fewer enamel lesions
progress to dentinal caries in a fluoridated area
than in a nonfluoridated area. F does not pre-
vent the initial carious attack, which would be
expected if its presence in the enamel crystal
increased enamel resistance to acid dissolution,
but rather the F in the oral cavity acts to inhibit
further demineralization of the lesion and to
promote its remineralization.
Fluoride and Saliva
Resting salivary F concentrations are low,
although they are some three times higher in
fluoridated than in nonfluoridated areas. In
a fluoridated area, salivary F levels averaged
0.016 ppm, whereas they were 0.006 ppm in a
nonfluoridated area.138 Fluctuation of salivary F
levels is normal, and after toothbrushing with
an F toothpaste or mouthrinsing with an F solu-
tion, salivary F levels can rise 100- to 1000-fold.
This level rapidly drops back to normal, and the
saliva is likely to be an important source of
plaque F during this time.150 The role of saliva
in caries inhibition is still not well defined.
Effects on Different Tooth Surfaces
One of the observations from early fluoridation
studies in the Netherlands and New Zealand
was that caries reductions were greatest for the
free smooth surfaces and proximal surfaces of
teeth and were less pronounced for pit-and-fis-
sure surfaces.12,110 Murray’s study of 15-year-
olds in naturally fluoridated Hartlepool and
nonfluoridated York, England, found that those
in Hartlepool had a mean DMF (decayed, miss-
ing, and filled) score of 4.96, whereas those in
York had a mean DMF of 8.95. However, the
number of carious approximal surfaces of
molars was 11 times greater in York.131 This pat-
tern of more pronounced effect on smooth sur-
faces than on pit-and-fissure surfaces has since
become a standard finding in studies in which
caries is recorded for tooth surfaces.11 It follows
that when DMFS (decayed, missing, and filled
surface) scores are declining in a population,
the proportion of all decayed surfaces that are
pit-and-fissure surfaces will increase, even
though the absolute number may diminish.
EFFECTIVE USE OF FLUORIDE
Categorizing F compounds into “systemic fluo-
rides” and “topical fluorides” is not easily done
because the line between these categories gets
blurred: “systemic” vehicles like water fluorida-
tion and F supplements have been shown to
have topical cariostatic action, and some “topi-
cal” vehicles like F toothpaste can be swallowed
inadvertently and have systemic effects (fluoro-
sis). As stated earlier, the evidence shows that
the most effective community-wide use of F is
in frequent, low-concentration intraoral expo-
sures such as in drinking water or tooth-
paste.4,57,113,178 Less frequent application of
high-concentration gels has its place in the care
of highly caries-susceptible patients.
The most cost-effective way of reaching an
entire community with regular, low-concentra-
tion F is through water fluoridation. This is true
public health action, and it is also one that has
stirred public controversy. The unique position
of water fluoridation as a public health action is
the subject of the next chapter.
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184. Whiting P, MacDonagh M, Kleijnan J. Association of
Down’s syndrome and water fluoride level: A system-
atic review of the evidence. BMC Public Health, web-
site: http://www.biomedcentral.com/1471-2458/1/6.
Accessed September 29, 2004.
185. Yiamouyiannis J, Burk D. Fluoridation and cancer:
Age-dependence of cancer mortality related to artifi-
cial fluoridation. Fluoride 1977;10:102-23.
186. Zipkin I, Likins RC. The absorption of various fluorine
compounds from the gastrointestinal tract of the rat.
Am J Physiol 1957;191:549-50.
187. Zipkin I, McClure FJ. Cariostatic effect and metabo-
lism of ammonium fluosilicate. Public Health Rep
1954;69:730-3.
188. Zipkin I, Scow RO. Fluoride deposition in different
segments of the tibia of the young growing rat. Am
J Physiol 1956;185:81-4.
 25 Fluoridation of Drinking Water
OPTIMAL FLUORIDE CONCENTRATIONS IN
DRINKING WATER
EARLY STUDIES OF FLUORIDATED WATER
WORLD STATUS OF FLUORIDATION
FLUORIDATION IN THE UNITED STATES
Role of Federal, State, and Local Governments
in Fluoridation
Drinking Water Standards
CARIES REDUCTIONS FROM FLUORIDATION
Reducing the Disparities
Caries Reductions in Children
Caries Reductions in Adults
Prenatal Benefits
Effects on the Primary Dentition
Fluoridation is the controlled addition of a flu-
oride (F) compound to a public water supply to
bring its F concentration up to a level that will
best prevent dental caries while avoiding
unsightly fluorosis. A related public health
measure is defluoridation, the process of
removing excess F naturally present in a water
supply to prevent dental fluorosis (or even
skeletal fluorosis in some parts of the world
where the naturally occurring F concentration is
high enough).
In our studies of F and its relationship to
dental caries, water fluoridation deserves special
attention. This is because the F-caries relation-
ship was first discovered in studies of communi-
ties with naturally fluoridated water and
because water fluoridation is the purest public
health use of F. Fluoridation is not a targeted
approach to caries prevention; its use means
that F reaches everyone in the community. This
feature is both the measure’s greatest strength
and its greatest problem in terms of social pol-
icy. This chapter describes the various issues
specific to water fluoridation as a means of con-
trolling caries at the community level.
326
Partial Exposure to Fluoridation
Caries Patterns When Fluoridation Ceases
FLUORIDATION IN THE AGE OF MULTIPLE
FLUORIDE EXPOSURE
ECONOMICS OF FLUORIDATION
Savings in Treatment Costs
POLITICS OF FLUORIDATION
Public Attitudes and Knowledge
Opposition to Fluoridation
Court Decisions on Fluoridation
Fluoridation Decisions at the Community
Level
THE FUTURE
The unit usually used in the United States for
expressing the F concentration in drinking
water is parts per million (ppm), although
countries using metric measurements usually
express it in milligrams per liter (mg/L).
Fortunately the numerical values are the same
in both measuring units; that is, 1.2 ppm is the
same as 1.2 mg/L. We use parts per million in
this book.
OPTIMAL FLUORIDE
CONCENTRATIONS IN DRINKING
WATER
Public policy for controlled water F levels in the
United States takes the form of nonenforceable
guidelines set by the U.S. Public Health Service
(Box 25-1). Current policy is that these levels,
for the United States, should be between 0.7
and 1.2 ppm F, depending on mean annual
temperature of the locality. These guidelines,
based on the assumption that people drink
more water in a hotter climate than they do in a
cooler one, are more than 40 years old and are
shown in Table 25-1.
 25 Fluoridation of Drinking Water 327

BOX 25-1 Who Watches Over How Much Fluoride Is in our Drinking Water?

Two agencies of the federal government are involved in overseeing levels of fluoride (F) in drinking water. At the
regulatory level, the Environmental Protection Agency (EPA) sets the legal upper limit at 4.0 ppm F. No one adds
fluoride to drinking water at that level, but it can occur naturally (although it is rare to find this high level in the United
States). If such an F concentration is found in a public water supply, the excess F must be removed or a new water
source found. Here the issue is human health. The EPA considers that 4.0 ppm F is the upper limit before the risk of
skeletal fluorosis becomes too high. This regulation has nothing to do with what the best concentration for caries
prevention might be.
In terms of guidelines for the best concentration for caries prevention, the U.S. Public Health Service recommends
that drinking water in the United States be fluoridated to a level between 0.7 and 1.2 ppm F, depending on climate. This
recommendation is nonenforceable.
The maximum contaminant level goal (MCLG) is the level of a contaminant in drinking water below which there is
no known or expected risk to health. MCLGs allow for a margin of safety and are nonenforceable public health goals.
The maximum contaminant level (MCL) is the highest level of a contaminant that is allowed in drinking water. MCLs
are set as close to MCLGs as is feasible when the best available treatment technology and cost are taken into
consideration. MCLs are enforceable standards. Both the MCLG and the MCL remain at 4.0 ppm F,46 pending further
review by the EPA.

Table 25-1 Fluoride levels recommended by the U.S. Public Health Service for cool and warm climates122
Recommended Control Limits of Fluoride Concentrations
(ppm)
Annual Average of Maximum Daily Air
Temperatures (Degrees F)* Lower Optimal Upper

50.0-53.7 0.9 1.2 1.7

53.8-58.3 0.8 1.1 1.5
58.4-63.8 0.8 1.0 1.3
63.9-70.6 0.7 0.9 1.2
70.7-79.2 0.7 0.8 1.0
79.3-90.5 0.6 0.7 0.8
*Based on temperature data obtained for a minimum of 5 years.

These temperature-related guidelines were
developed from a series of well-conducted epi-
demiologic studies performed in the American
west during the 1950s51-54; from these data, the
researchers produced an algebraic formula for
determining a community’s optimal water F
level. This formula is based on Dean’s conclu-
sion (see Chapter 24) that 1.0 ppm F was the
optimum concentration for the Chicago area.
Regardless of how appropriate Dean’s conclu-
sion was in his time, the appropriateness of
temperature-related guidelines is questionable
given today’s living conditions. The climate-
related guidelines are widely ignored in the
United States anyway.80
The temperature-related guidelines in Table
25-1, developed under American dietary and
cultural conditions, have been found unsuit-
able for Asian and African regions. Hong Kong,
for example, reduced its water F levels to 0.5
ppm F by the mid-1990s because of increased
fluorosis, and an expert committee of the World
Health Organization has recommended a range
of 0.5-1.0 ppm F for all parts of the world.130
The recommended levels for the United States
have been in place since 1962 and are due
for revision, because much in our lifestyles
and exposure to F has changed since then. For
example:
●
Air-conditioning is widespread and has
been a major factor in promoting popula-
tion growth in hotter parts of the country.
Because we live in an increasingly climate-
controlled environment, the original prem-
ise that people drink more water in hotter
parts of the country becomes weaker.65,113
328 The Distribution of Oral Diseases and Conditions
●
There has been a huge increase in con-
sumption of soft drinks and bottled waters
(see Chapter 28). These may or may not be
made with fluoridated water, and products
from the same plant can be distributed to
both fluoridated and nonfluoridated areas.
●
An increase in the prevalence of fluorosis
since the time the guidelines were devel-
oped (see Chapter 24) indicates that young
people are ingesting more F than they used
to. Increased use of commercial juice
drinks in place of milk and water could be a
factor.83
Like all guidelines for F use, the temperature-
related recommendations for F levels in drink-
ing water need periodic monitoring, because the
world has changed since they were developed.
EARLY STUDIES OF FLUORIDATED
WATER
The most important early studies of fluoridated
water were described in Chapter 24. All the early
research on the safety of F use and its impact on
human health and function studied F in drink-
ing water. By the time the first controlled fluori-
dation trials were begun in 1945, research had
established the following facts:
●
The healthy human body possesses a prompt
and efficient excretory mechanism for F that,
at least at the low F levels usually found natu-
rally in drinking water in the United States,
minimizes the danger of long-term accumula-
tion.
●
Although ingested F is partly deposited in
bone, and although skeletal F concentrations
increase with age, skeletal damage could not
be demonstrated in users of F-bearing domes-
tic water in the United States.
●
No impairment in general health could be
found among people who had drunk water
with up to 8 ppm F for long periods of time.
Four independent studies of controlled
fluoridation, in which the F concentration in
the water supplies of the communities was
brought up from negligible levels to 1.0-1.2
ppm, were begun in 1945 and 1946. They fol-
lowed a long series of epidemiologic studies of
caries experience related to F concentration in
drinking water, which were summarized in
Chapter 24. The four communities originally
studied were the following:
1. Grand Rapids, Michigan. This study was
begun in January 1945 with nearby
Muskegon as the control city and was
directed by Dean and his colleagues.30
2. Newburgh, New York, with Kingston as
the control city.4
3. Evanston, Illinois, with Oak Park as
control.13
4. Brantford, Ontario, with Sarnia as control.
Naturally fluoridated Stratford, Ontario,
was also included in this study.68
At the end of terms ranging up to 15 years,
caries experience was shown to be sharply
reduced in each of the study populations,
despite some differences in study design and
examination criteria.2,5,12,69 These pioneer stud-
ies also found that dental fluorosis occurred
to about the same extent6,105 as Dean had
described earlier28: namely, some 7%-16% of
the population was found to have mild to very
mild fluorosis when the F exposure came from
drinking water containing 1.0 ppm F.
The four original studies in which F was
added to drinking water are sometimes called
“classic” studies, although “pioneering” might
be a better term. By present-day standards of
field trials they were rather crude. Although
they are often referred to as “longitudinal”
studies, none of them was; all were of sequen-
tial cross-sectional design. Sampling methods
and dental examiners tended to vary from year
to year,1 which risked bias and unnecessary
random error. Methods of statistical analysis
were primitive by today’s standards. Data from
the control communities were largely neglected
after the initial reports, and conclusions were
based on the much weaker before-after analysis
in the test cities. (Among the early studies, the
only true longitudinal study of fluoridation’s
effects was the Tiel-Culemborg study in the
Netherlands.)8,9
Perhaps too much emphasis has been given
to these four pioneering studies, for they really
just confirmed prospectively what had already
been demonstrated through Dean’s research,
which still stands as a model of how to apply
the epidemiologic method. But despite the
design flaws in the original four studies, it is
difficult for an open-minded observer to reject
their conclusions that fluoridation was effec-
tive in reducing the prevalence and severity
of caries.
 25 Fluoridation of Drinking Water 329

Public policy on any issue usually has to be
established without complete information, and
water fluoridation is no exception. When one
considers that adults, on average, ingest 1-3 mg
F/day in their normal diets, that 9-10 million
Americans (and many other peoples around the
world) have been drinking naturally fluoridated
water for a century or so, and that over 100 mil-
lion Americans have been drinking F-supple-
mented water for generations, there is a lot of
empirical evidence that fluoridation at 1 ppm is
not harmful. Certainly there is no credible evi-
dence that F in these amounts leads to serious
ill health. The scientific method cannot prove a
negative; we take inability to reject the null
hypothesis for specific conditions (see Chapter
13) as evidence of safety. The occasional allega-
tion of a sensitivity reaction should be investi-
gated seriously, but with the passage of time the
probability becomes greater that fluoridation at
1.0 ppm produces no undesirable side effects.
We support the policy of the U.S. Public Health
Service that F should be added to drinking water
at the recommended concentrations.
WORLD STATUS OF FLUORIDATION
Unfortunately there is no central compendium
for international data on populations receiving
fluoridated water. The FDI World Dental
Federation has some self-reported information
for some countries on its website (http://www
fdiworlddental.org), but the data are not col-
lated. Older information from the FDI shows
that in 1984 there were 34 countries reporting
fluoridation projects reaching some 246 mil-
lion people, not including areas with naturally
occurring F in the drinking water. Both the
British Fluoridation Society16 and the World
Health Organization95 estimated that some 210
million people worldwide receive fluoridated
water. The foregoing statements are all of uncer-
tain validity. Some factual summary statements
about the global distribution of fluoridation are
shown in Box 25-2.
Ireland remains the only nation (apart from
the city-state of Singapore) to have a mandatory
fluoridation law. Enacted in 1960, it subse-
quently withstood a legal challenge that went to
the Irish High Court. Most large Irish urban
communities had fluoridated water in the
period 1964-72; 71% of Ireland’s population
resided in fluoridated areas by 2004.98
Information from the Pan American Health
Organization shows that nine countries in
South America and the Caribbean have water
fluoridation; most notable are Brazil and Chile,
with 42% of the population in each country
receiving fluoridated water.
At the other end of the spectrum, fluoridation
has made little headway in Europe, and it is not
technically feasible for much of Asia and Africa
because of the relative absence of municipal
water systems there. In Europe, fluoridation in
the socialist countries of Eastern Europe ended
with the demise of the former Soviet Union
in the early 1990s.79 In Britain, the city of
Birmingham, the second largest British city, has

BOX 25-2 Summary of Global Distribution of Water Fluoridation in 2000

●
In 1984, the FDI World Dental Federation reported that 34 countries had some fluoridation projects, which reached a
total of 246 million people.
●
In the city-state of Singapore, fluoridation in 2004 reached virtually 100% of the population. The only other nation
with a mandatory fluoridation law is Ireland, where over two thirds of the population now receives fluoridated water.
●
Fluoridation reaches more than 50% of the population in Australia, Ireland, Malaysia, New Zealand, and the United
States.
●
In Europe, some 10% of the population of Spain and the United Kingdom receive fluoridated water. Principal cities
fluoridated are Sevilla and Córdoba in Spain, and Birmingham and Newcastle in the United Kingdom.
●
Previously reported fluoridation projects in eastern European countries are of uncertain status since the breakup of
the Soviet Union in 1989-91. Those in the former East Germany are known to have ceased since German
reunification in 1989.
●
Extensive water fluoridation projects previously reported in South and Central America are of uncertain status.
330 The Distribution of Oral Diseases and Conditions
been fluoridated since 1964, and there is a belt
of fluoridated communities near Birmingham in
the West Midlands. On the other hand, there is
no water fluoridation at all in Austria, Belgium,
Denmark, France, Germany, Italy, Norway, and
Sweden. Specific bans are in place in Sweden
and Denmark (where a law on additives is inter-
preted to exclude fluoridation), and for various
reasons fluoridation is a dead political issue in
the others.
In Europe a notable setback, as opposed to
lack of progress, came in the Netherlands, where
fluoridation at one point reached 3 million peo-
ple but was halted by the government of the
Netherlands in 1976. The long-fluoridated
Finnish city of Kuopio also ceased fluoridating
in 1992, as did the city of Basel in Switzerland
in 2003.
FLUORIDATION IN THE UNITED
STATES
The Division of Oral Health of the Centers for
Disease Control and Prevention (CDC) in
Atlanta maintains fluoridation surveillance for
the United States. The Water Fluoridation
Reporting System, a voluntary program, for-
wards data from the states to the CDC, which
then publishes the information periodically on
its website. Extent of fluoridation is one of the
eight indicators used in the National Oral
Health Surveillance System (see Chapter 4).
At the end of 2000, the CDC estimated that
fluoridated water was reaching some 162
million people in the United States, 57% of
the total population and 66% of those receiv-
ing municipal water.125 About 10 million of
these people were receiving water naturally
fluoridated at 0.7 ppm F or more; the greatest
concentrations of naturally fluoridated com-
munities are found in Texas, Illinois, and New
Mexico.128 In the year 2000 there were over
10,000 water systems with controlled or natural
fluoride levels of 0.7 ppm F or more; these rep-
resent 18% of all public water systems in the
country. This may not sound like much, but a
large majority of public water systems serve
communities with fewer than 1000 people, so
that fluoridation is not cost effective. Drinking
water is fluoridated in 42 of the 50 largest
American cities. Over 700 communities in the
United States have been fluoridating the water
for 30 years or longer, and many of the natu-
rally fluoridated communities have been using
the same water source for more than three gen-
erations. The proportion of state populations
reached by fluoridation ranges from close to
100% in Minnesota, Kentucky, Indiana, and
Tennessee (plus the District of Columbia) to
2% in Utah and 9% in Hawaii.
Role of Federal, State, and Local
Governments in Fluoridation
The decision to fluoridate is usually made by
the local community, although a number of
jurisdictions can be involved when water service
district boundaries do not coincide with city
and county boundaries. State laws requiring
fluoridation now stand in 10 states; at the other
end of the spectrum, there are three states that
have laws requiring referenda. These states are
shown in Table 25-2. The fluoridation laws have
been generally successful, because in all states
with them a high proportion of the population
is receiving fluoridated water. Some of the states
listed in Table 25-2, however, have provisions in
their laws that can frustrate progress. These pro-
visions reflect the political compromises neces-
sary to get the law passed. For example, the
California law, passed after a vigorous political
battle in 1996, cannot be enforced unless out-
side funds (i.e., state or federal funds) are made
available to the local community for the pur-
chase, installation, and operation of the fluori-
dation system.
The U.S. Public Health Service, initially
through its Division of Dental Health (now
defunct) and later through the CDC, has pro-
vided funds and consultative expertise to pro-
mote fluoridation through several mechanisms.
Federal funds were available through the
Division of Dental Health in 1965-67, and 13
states used them to begin fluoridation projects.
These funds were specifically earmarked for
fluoridation but were cut repeatedly as the cost
of the Vietnam War (1955-75) increased.
Funding was revived from 1978 to 1981, when
the CDC had a budget of up to $9 million per
year for distribution to states and communities
for fluoridation. Some 765 communities, with a
population of nearly 11 million, benefited
directly during this period.
In 1981 seven block grants were initiated as a
method of distributing federal health funds to
 25 Fluoridation of Drinking Water 331

Table 25-2 States of the United States with fluoridation laws requiring fluoridation in 2004*
Size of Community Exemption Maximum Natural F Level to Be
State Year Started Affected Provision? F Level (ppm) Maintained

CT 1965 20,000+ No 0.8 0.8-1.2

MN 1967 All No — 0.9-1.5
IL 1967 All No 0.8 0.9-1.2
SD 1969 500+ No 0.9 0.9-1.7
OH 1969 5,000+ No — 0.8-1.3
GA 1973 All incorporated Public vote — No higher than
1.0 ppm
NE 1973 All political subdivisions Public vote 0.7 0.8-1.5
CA 1996 10,000 service connections No 0.7 0.7-1.2
DE 1998 All No — 0.8-1.2
NV 1999 Counties with 400,000+, No — 0.7-1.2
with either a water system
serving 100,000+ or a
water authority
Data from the Centers for Disease Control and Prevention, personal communication, 2004.
*Three states have laws that require a favorable vote of the local community before fluoridation can be implemented; these are ME (1957),
NH (1959), UT (1976, revised 2003).

BOX 25-3 Sources of Federal Government Funding for Fluoridation

●
Preventive Health and Health Services Block Grant funds are awarded to states, although in 2002 only 2% of the
$128 million granted to states was used for fluoridation.126
●
Health Resources and Services Administration in 1998 funded six projects in six states for 3 years to develop their
fluoridation programs and promote fluoridation. Four of these six awards were to state health departments, one was
to a county health department, and one was to a nonprofit organization.123
●
The Centers for Disease Control and Prevention (CDC) in 1999 awarded 3-year grants to 13 states or tribes for
fluoridation. In 2001 and 2002, the CDC funded 5-year cooperative agreements with 12 states and one territory for
state oral health program core capacity, including administration of state fluoridation programs. These jurisdictions
were Alaska, Arkansas, Colorado, Illinois, Michigan, Nevada, New York, North Dakota, Oregon, Rhode Island, South
Carolina, Texas, and the Republic of Palau. Four of these (Colorado, Illinois, Nevada, Texas) were also among the
1999 recipients. Two of these states received additional funds for fluoridation equipment.127

the states. The philosophy behind block grants
is that funds to finance a host of federal categor-
ical programs that have grown up over the years
are lumped together in specific blocks, and
recipient states can determine for themselves to
which programs they will allocate the funds.
The Preventive Health and Health Services
Block Grant includes funds for fluoridation, but
fluoridation projects then have to compete at
the intrastate level against other worthy preven-
tion causes such as hypertension control and
emergency medical services. Recent sources of
federal funding for fluoridation are listed in Box
25-3. Future funding remains uncertain.
Drinking Water Standards
The U.S. Environmental Protection Agency
(EPA) is the regulatory agency with responsibility
for setting national standards for acceptable
drinking water under the Safe Drinking Water Act
(Public Law 93-523; see Box 25-1). This act was
first passed in 1974 and has been renewed sev-
eral times since. Most of these standards deal
with defining acceptable levels of bacterial and
332 The Distribution of Oral Diseases and Conditions
chemical contaminants. In the 1975-76 National
Interim Primary Drinking Water Regulations, in
the standards promulgated soon after passage of
the legislation, the EPA referred to naturally
occurring F above 2 ppm as a “contaminant”
requiring removal from drinking water. This lat-
ter requirement was intended to reduce dental
fluorosis in affected areas, but it was criticized by
many of the local authorities concerned on the
grounds of cost (defluoridation is more expen-
sive than fluoridation). Many communities that
used drinking water naturally fluoridated at
more than 2 ppm were small and could not
afford the cost of meeting the standard. In addi-
tion, few of them seemed interested in defluori-
dating: the resulting fluorosis did not concern
them and they were not aware of any other ill
effects, so why bother?
The Interim Primary Drinking Water Regula-
tions of 198040 left the recommended maximum
contaminant level (RMCL) at 2 ppm F but
included an explanatory statement that this
standard did not contradict the beneficial effects
of F in reducing dental decay. Whether this state-
ment really helped clarify things, especially
because that unfortunate word contaminant was
retained, is doubtful. Public discussion on estab-
lishing the final standards became intense dur-
ing the mid-1980s; the EPA was deluged with
demands from both proponents and opponents
of fluoridation. The state of South Carolina, for
whom compliance with the RMCL of 2 ppm F
would have been very expensive, brought suit
against the EPA in 1981 to attempt to force it to
revoke the interim RMCL. The EPA, in response,
promised to rule on the issue when its studies
were complete. South Carolina sued again in
1984, seeking faster action from the EPA, and
this led to issuance of a consent decree in January
1985.41
Eventually the EPA settled this seemingly
irresolvable issue by ducking underneath it.
Concluding after its studies that dental fluorosis
in the United States was a cosmetic defect rather
than a health problem, the EPA proposed an
RMCL for F of 4.0 ppm F, on the grounds that
this level was sufficiently low to protect against
crippling skeletal fluorosis.42 By late 1986, this
RMCL became the maximum contaminant level
for 4.0 ppm F, meaning that the EPA now had a
standard to enforce. The original level of 2.0
ppm F became a secondary standard; that is, it
was a nonenforceable recommended maxi-
mum, in effect a guideline. This secondary stan-
dard was justified on the grounds that “2 mg/L
would prevent the majority of cases of water-
related cosmetically objectionable dental fluo-
rosis while still allowing for the beneficial
effects of F (prevention of dental caries).”43
Although some aspects of this debate resem-
bled a Gilbert and Sullivan operetta, it raised
the serious question of whether control of den-
tal fluorosis should be a subject for national
standards or whether the issue should be left to
states or localities to handle. State dental direc-
tors have to carry much of the regulatory load,
and many are unhappy with the requirement
that local communities must be notified when
their F levels are between 2 and 4 ppm, espe-
cially since the EPA mandates that the word con-
taminant (again!) must appear in the letters of
notification.44
Standards of this sort quite properly need
reexamination from time to time. In 1992, the
EPA requested the National Research Council to
review the issue of primary and secondary stan-
dards for F in drinking water. An expert com-
mittee whose members had a variety of
backgrounds (most were from outside dentistry)
worked for more than a year and concluded that
there was no current evidence to justify a change
in the standards.90 The committee recom-
mended that the issue of the relationship of F
exposure to health be revisited at regular inter-
vals because new evidence was appearing con-
tinuously. Following this report, the EPA
decided in late 1993 not to change what was
then called the maximum contaminant level goal
of 4.0 ppm F.45 This standard still holds.46
CARIES REDUCTIONS FROM
FLUORIDATION
For many years, the statement that “water fluor-
idation reduces dental caries experience by half”
was hardly questioned within dentistry. At a
time when drinking water was the only signifi-
cant source of F, that statement was probably
true enough. Its basis was Dean’s 21 cities epi-
demiologic study of naturally fluoridated
areas,29,31 supplemented by the results of
the initial four controlled fluoridation projects
begun in 1945-46. A summary of the results of
these four pioneering studies is presented in

Table 25-3 Decayed, missing, and filled (DMF) teeth per child ages 12-14 years and missing teeth per
child at the end of the study term in four pioneer fluoridation communities5
Mean DMF Teeth
Community Year per Child
Grand Rapids (F) 1944-45 9.58
1959 4.26
Evanston (F) 1946 9.03
1959 4.66
Sarnia (non-F) 1959 7.46
Brantford (F) 1959 3.23
Kingston* (non-F) 1960 12.46
Newburgh* (F) 1960 3.73
Note: Fluoridated communities are designated by F, nonfluoridated by non-F, after city name.
*Children in Kingston and Newburgh were ages 13-14 years.
Table 25-3. The table shows that after 13-15
years of fluoridation, DMF (decayed, missing,
and filled) scores in 12- to 14-year-old perma-
nent-resident children favored fluoridation by
48% to 70%. In absolute terms, average DMF
levels in the fluoridated communities dropped
from 7-9 teeth at the start of the studies to 3-4
teeth per child after 13-15 years.
Since those studies, exposure to F from
toothpaste, other dental products, and food and
drink has become universal. As a result, water
fluoridation has moved from being the sole F
exposure, as it was in those early days, to one of
a number of F exposures. Caries status overall
has continued to improve, and overall F expo-
sure has to take much of the credit for that.
Another reason for the inability to attribute
50% reductions in caries to water fluoridation
today is that the effects of F in drinking water
diffuse into surrounding communities and raise
the baseline. Nonetheless, 12-year-old children
living in states where more than half of
the communities have fluoridated water have
26% fewer decayed tooth surfaces per year than
12-year-old children living in states where less
than one quarter of the communities are fluori-
dated.61 A rigorous systematic review in Britain,
carried out by an expert group at the University
of York, concluded that the median increase in
the proportion of persons with DMFT score
(number of decayed, missing, and filled perma-
nent teeth) of 0 attributable to water fluorida-
tion was 15%.85 Because the review had strict
criteria for inclusion and exclusion of studies,
this conclusion was reached from a fairly small
number of studies. (One of the conclusions of
25 Fluoridation of Drinking Water 333
Percent Missing Teeth Percent
Difference per Child Difference
55.5 0.84 65.6
0.29
48.4 0.19 68.4
0.06
0.75
56.7 0.22 70.7
0.92
70.1 0.10 89.1
the systematic review was that the large body of
literature on the effectiveness of water fluorida-
tion was generally of poor quality, as was the lit-
erature claiming harm from fluoridation.)
It would thus be unreasonable to expect con-
tinuation of 50% reductions in caries levels
from fluoridated water alone; the generally
reduced caries levels we enjoy are today a result
of total F exposure from all sources. The contin-
uing importance of water fluoridation as a cor-
nerstone of public policy, however, is indicated
by the fact that the CDC lists it as one of the top
10 public health achievements of the twentieth
century.124
Reducing the Disparities
Disparities refers to the differences in health sta-
tus between favored and unfavored groups in
our society, usually racial-ethnic groups and
those of different socioeconomic status (SES).
Disparities are a complex and persistent prob-
lem, with economic costs as well as political
and moral overtones. Fluoridation has the
major social advantage of benefiting children in
lower SES areas relatively more than those in
higher SES areas.10,19,57,73,97,100 An example is
shown in Fig. 25-1, which presents data from
the most recent clinical examinations in the
Newburgh-Kingston studies in New York. When
caries levels found in 7- to 14-year-old poor and
nonpoor children in the 1995 examinations
were compared, the greatest disparity was seen
between the poor and nonpoor in nonfluori-
dated Kingston rather than between poor
groups in the two cities. Reducing the disparities
in health status between high- and low-SES
334 The Distribution of Oral Diseases and Conditions
1.6
Mean no. permanent teeth affected
1.2
0.8
0.4
0 relatively few fluoridated areas, so that the diffu-
Newburgh Newburgh
non-poor poor
Fig. 25-1 Caries experience, expressed as covariate-
adjusted mean decayed, missing and filled surfaces per child
in 7- to 14-year-old children in Newburgh and Kingston, New
York, by poverty status (“poor” children were defined as those
participating in the school lunch program).77 (From Burt BA:
Fluoridation and Social Equity. J Public Health Dent 2002;
62:195–200. Reproduced by permission of the Journal of
Public Dentistry.)
areas is a United States national health objective
for 2010, and fluoridation does its part to help
achieve this goal.
The most searching assessment of fluorida-
tion’s effectiveness, including its effectiveness
in reducing disparities between groups, came
with the systematic review carried out by the
Centre for Reviews and Dissemination at the
University of York in Britain in 2000 and
referred to earlier.85 This review is the most rig-
orous scrutiny of existing data on fluoridation
yet carried out. It has been criticized by both
proponents and opponents of fluoridation
because the stringent inclusion and exclusion
criteria led to the omission of many reports
from consideration. One of the aims of this
exhaustive review was to determine if fluorida-
tion reduced the disparity in caries experience
between higher and lower SES groups. Most of
the 15 papers selected to examine this question
reported data for 5-year-old children. The
review found no difference between fluori-
dated and nonfluoridated areas in the magni-
tude of the disparities between children of
different SES groups when caries prevalence
was measured. However, a favorable reduction
in differences between social groups was seen
when caries severity was the measure. Data for
ages other than 5 years were too limited to per-
mit conclusions.
Caries Reductions in Children
Studies of the effectiveness of fluoridation in
reducing caries experience in children far out-
number studies of its effectiveness in adults. The
many fluoridation studies conducted in different
parts of the world have varied in quality of
design and operation, but their results have still
been remarkably uniform. Differences in oral
health between fluoridated and nonfluoridated
areas are easier to demonstrate when there are
Kingston Kingston sion effect (see earlier) has less impact. In
non-poor poor Britain, where water fluoridation is not wide-
spread, reductions of around 50% are still found
in primary and mixed dentitions.15,47,58,74,116,120
Similar results have been reported in Brazil27; in
Australia, where comparisons were based on
school dental service data for groups of 9000 or
more children111,112; in New Zealand121; and in
Ireland.93
Where fluoridation is widespread, as in the
United States, differences in caries experience
between children in fluoridated and nonfluori-
dated communities are now estimated to be
more on the order of 18%-35%.17,26 However,
how much of F’s benefits is due to water fluori-
dation, rather than to overall F exposure, really
cannot be estimated with any precision now for
the following reasons:
●
The development and almost universal use
of fluoridated toothpaste and other dental
products containing F, plus the presence of
F in food and beverages processed with
fluoridated water, means that there are
many different F exposures for the average
American.
●
The extreme mobility of the U.S. popula-
tion means that most people have had
varied exposures to fluoridated water
at different times of life. When this is
added to the diffusion effect (described
earlier), it is clear that there is no way of
finding true control subjects in the United
States.
●
History of exposure to fluoridation is diffi-
cult to document in research studies. There
are no biomarkers for lifetime exposure,
and interview data can be unreliable.

Caries Reductions in Adults
The caries-inhibitory effects of F are not con-
fined to childhood. Contrary assumptions were
surprisingly common in light of the evidence in
Chapter 24 and stemmed from beliefs that (1)
the primary cariostatic action of F was preerup-
tive, and (2) caries was a disease of childhood.
Neither of these beliefs is viewed as true today.
Over a lifetime, fluoridation reduces coronal
and root caries.60,91
Studies of fluoridation’s effects in adulthood
began early with McKay’s recognition that
45-year-old adults benefitted from consum-
ing fluoridated water.86 Adults born and raised
in naturally fluoridated Colorado Springs were
found to have 60% lower mean DMF scores than
their counterparts in nonfluoridated Boulder.
Residents of Colorado Springs also had far fewer
teeth missing.104,106 Similar findings among
adults came from Aurora, Illinois, a city with 1.2
ppm F naturally occurring in its drinking
water.39 Both the Colorado Springs and the
Aurora studies went to considerable lengths to
confine the analysis to permanent residents, to
assess lifetime effects of exposure to fluoridated
water. In light of today’s questions about
preeruptive and posteruptive cariostatic effects
of F, it is a pity that the deliberate exclusion of
study subjects who moved into the fluoridated
areas after childhood precluded any considera-
tion of this issue. It is also unfortunate that nei-
ther study assessed the SES of the people
concerned. In fairness, sensitivity to the impact
of SES on health status (see Chapters 20 and 21)
was not as sharp at the time of these studies as it
is today, but the net effect is to diminish their
value in the perspective of history.
A later study did use more detailed statistical
analysis in evaluating data from Lordsburg (3.5
ppm F) and Deming (0.7 ppm F), New Mexico.
SES status was higher in Deming. Results still
favored the community with the higher F level.
After other important variables were controlled
for, Deming adults were found to have two
more restored teeth per person than did those
in Lordsburg, although fluorosis was naturally
more severe in Lordsburg.36 The DMFT data for
these two communities are shown in Fig. 25-2.
Root caries is also less prevalent in fluori-
dated areas than in nonfluoridated areas.21,115
This finding is important, because with increas-
25 Fluoridation of Drinking Water 335
ing tooth retention in an aging population the
amount of root caries would otherwise be
expected to increase and become a greater treat-
ment problem in the future. It is not yet clear
whether F’s protective effect against root caries
is due to topical action on exposed root sur-
faces, to incorporation of F into cementum
before root exposure in the oral cavity, or to a
combination of both.
Prenatal Benefits
The policy issue of whether prenatal exposure
to F actively promotes caries resistance in the
infant is related to the use of supplements and
is discussed in Chapter 26. F ingested by the
mother crosses the placenta and enters the fetal
circulation.94,114 The fetal plasma F level is cor-
related with the maternal level, although it is
somewhat lower, probably because much of
the F is taken up by the rapidly mineralizing
skeleton and teeth of the fetus.94 The pertinent
question is whether the developing primary
dentition has enhanced resistance to caries
because of this additional F.
Some support for a prenatal exposure benefit
came from the Evanston fluoridation study, in
which children who were exposed to fluori-
dated water in utero as well as postnatally were
reported to have fewer carious lesions than
those who received it only postnatally.11 Other
authorities, however, did not find this effect.8,67
A comprehensive 1981 review concluded that
there was probably no benefit in prenatal F
exposure, though it was not ruled out com-
pletely.34 If the offspring derives any benefit at
all from prenatal F exposure, such benefit
would be slight.
The absence of prenatal exposure benefits is
a part of the discussion of preeruptive versus
posteruptive effects in determining how F
works. Benefits or lack of them aside, it is clear
that fluoridation is quite safe for the developing
fetus. No special precautions are therefore nec-
essary for expectant mothers in fluoridated
areas.
Effects on the Primary Dentition
Early fluoridation studies reported caries reduc-
tions in the primary dentition of about the same
range as was found in the permanent den-
tition.5,66,119 More recent British data show
that this range of caries reduction attributable to
336 The Distribution of Oral Diseases and Conditions

12

Filled D D

Missing
10
Decayed

L D
8
Mean DMFT

D
L L
6
L

0
27-40 41-50 51-65 All ages

Years

Fig. 25-2 Decayed, missing, and filled teeth (DMFT) in adults ages 27-65 in Deming (D; 0.7 ppm F in drinking
water) and Lordsburg (L; 3.5 ppm F in drinking water), New Mexico.36

fluoridation is being maintained.15,24,25,35,50,72,89 partial exposure to fluoridated water in adult-

The primary dentition clearly benefits from expo-
sure to fluoridated drinking water.
Partial Exposure to Fluoridation
A concentration of about 1.0 ppm F is regarded
as optimum for caries prevention in a moderate
climate. What happens in those communities
with water naturally fluoridated at suboptimum
levels, such as 0.4-0.7 ppm F? Dental benefits
still are found and are generally proportional to
the F concentration. A decision as to whether
fluoridation is worthwhile in a community
whose water contains, say, 0.6 ppm F is not eas-
ily made, for it is not certain whether the cost of
fluoridating is worth the additional dental ben-
efits expected.
The United States and Canada are highly
mobile societies. Many people have therefore
spent part of their lives in a fluoridated area and
part in a nonfluoridated area. The benefit of
hood has not been documented, but there is
evidence that partial exposure in childhood
reduces caries experience in proportion to
the length of exposure.5,6 In nonfluoridated
Coldwater, Michigan, children who had moved
to Coldwater after some residence in a fluori-
dated area had lower caries experience than did
those who had lived in Coldwater all their
lives.20 A British study demonstrated a 27%
reduction in caries incidence over 4 years
among children who were 12 years old when
fluoridation began in their community, relative
to the incidence in control children in nonfluo-
ridated areas.64
The evidence regarding partial exposure to
fluoridated water indicates that a cariostatic
benefit will be received that is more or less
proportional to the extent of the exposure.
Maximum benefit naturally comes with lifetime
exposure.

Caries Patterns When Fluoridation
Ceases
At the time when drinking water was the only
important source of F, there was evidence from
four communities in which fluoridation was
started and stopped some years later that caries
diminished with fluoridation and then increased
again after fluoridation stopped. Two of these
four communities were in Scotland, one was
in Germany, and one in Wisconsin.32,78,81,117 In
Wick, Scotland, there was a particularly notice-
able increase in caries prevalence after fluorida-
tion ceased in 1979.117
More recent instances of caries patterns fol-
lowing the cessation of fluoridation, all in the
modern era of multiple exposures to F, have
given rather different results. In British
Columbia, Canada, caries in a high-SES city con-
tinued to decline after fluoridation ended, a
finding largely attributed to the anticariogenic
effects of other F sources.84 Similar patterns have
been reported in Europe, both in the permanent
dentition79,107 and in the primary dentition,108
and these patterns are consistent with those of
the Tiel-Culemborg study (see Fig. 25-3). In the
30
Fluoridation
1953-1973
25
20
Mean DMFS
15
10
0
1968-69 1979-80
Year of examination
Fig. 25-3 Decayed, missing, and filled tooth surfaces (DMFS) in 15-year-old children in Tiel and Culemborg, the
Netherlands, before fluoridation ended in Tiel and for 15 years thereafter. The drinking water of Tiel was fluoridated
between 1953 and 1973.75
25 Fluoridation of Drinking Water 337
United States, cessation of fluoridation for 11
months led to no discernible change in caries
patterns. Again, this was in a high-SES commu-
nity in which regular use of F toothpaste was
the norm.22
Fluoridation ended in 1973 in Tiel, the test city
in the landmark Tiel-Culemborg study in the
Netherlands. At the time, caries experience was far
more favorable in fluoridated Tiel than in
Culemborg. But 15 years after fluoridation ended
in Tiel, the caries experience of Culemborg chil-
dren looked better.75 This finding illustrates the
importance of constant exposure to F (in this case
through fluoridated water) for full dental bene-
fits, as well as the effectiveness of other F expo-
sures, most notably the widespread use of F
toothpaste since the mid-1970s. (Because
Culemborg was of higher SES than Tiel, it would
be expected that use of F toothpaste among its
inhabitants would be greater.) These changes in
caries among children in Tiel and Culemborg, rel-
ative to fluoridation and subsequent exposure to
F toothpaste, are shown in Fig. 25-3. Had water
fluoridation continued in Tiel, we would expect
caries experience in that city still to be better than
that in Culemborg, but we will never really know.
Tiel
Culemborg
1981-82 1983-84 1985-86 1987-88
338 The Distribution of Oral Diseases and Conditions
The continued decline in caries experience
after fluoridation ceases would be expected in
communities in which there is regular and fre-
quent exposure to F from toothpaste and other
sources, whereas a caries increase would be
expected if drinking water were the only F
source. These findings emphasize yet again that
regular exposure to low-concentration F is what
leads to reduced caries experience, not necessar-
ily exposure to any one F vehicle. Water fluori-
dation is the most efficient way to bring F to a
community, but other exposure methods work
as well.
FLUORIDATION IN THE AGE OF
MULTIPLE FLUORIDE EXPOSURE
With caries levels at their lowest ever and F
available from a variety of sources, the question
arises of whether water fluoridation is still
needed. The answer is clearly, “Yes, it is.”
Although overall caries experience in the popu-
lations of the United States, Canada, western
European nations, Australia, and New Zealand
continues to diminish, we have noted that the
caries-preventive effects directly attributable to
water fluoridation are not as high as they once
were. The pioneering four studies reported
caries reductions of 50%-70% (see Table 25-3),
whereas more recent studies of fluoridation’s
effects produce less clearcut differences.33,70,82
The prime reason that effects attributable to
water fluoridation are reduced while overall
caries experience still continues to decline is
that an increase has occurred in exposure to F
from other sources. The main such source is F
toothpaste, but there are also possibly signifi-
cant amounts of F in processed foods and bever-
ages. The rise in the prevalence of fluorosis (see
Chapter 22) also attests to a broad increase in F
exposure.
On the other hand, some recent studies of
fluoridation’s effects in Britain and Australia
have yielded results that still show caries experi-
ence to be significantly lower in fluoridated
communities.38,47,101,111 One theory put for-
ward to explain these mixed results is that the
clear benefits of water fluoridation tend to be
seen more in places where fluoridation is less
common, which thus reduces the diffusion
effects61 and emphasizes the impact from water
fluoridation. The standard method of measur-
ing exposure to fluoridated water has tradition-
ally been ecologic: that is, if you live in a fluori-
dated community you drink fluoridated water;
if you live in a nonfluoridated community
you do not. This may have been adequate in
earlier days, but in today’s world of high mobil-
ity, heavy consumption of soft drinks and bot-
tled water, extensive use of water softeners
(which can take F from water), and high con-
sumption of processed foods, the ecologic
approach becomes increasingly questionable in
research design.
With differences in caries levels between
fluoridated and nonfluoridated communities
becoming increasingly blurred, the decision to
fluoridate a water supply is not always as auto-
matic as it once was. It can be argued that, when
caries experience is already low, good F expo-
sure comes from other sources, and the eco-
nomic cost of installing fluoridation is high,
then fluoridation is unnecessary. However,
there are two good reasons to argue for fluorida-
tion except in the most exceptional circum-
stances. One is the cost effectiveness of the
measure compared to other methods of caries
control (discussed in the next section), and the
second is the social equity benefits of fluorida-
tion. Alone among caries control strategies,
fluoridation reaches everyone in a community,
and as described earlier it has been shown to
reduce the strong SES gradient (see Chapter 20)
usually seen in caries distribution. Caries is still
more prevalent and severe in lower SES groups
than in higher SES groups in fluoridated com-
munities, but the differences are much less
marked than they are in nonfluoridated com-
munities (see Fig. 25-1). This factor of social
equity alone is a strong argument for fluoridat-
ing a community’s drinking water.
ECONOMICS OF FLUORIDATION
People look at the costs of fluoridation in differ-
ent ways. A city manager will be concerned
about the impact of equipment and operating
costs on the city’s budget—a subject that can
make any city council nervous. Proponents of
fluoridation stress the impressive cost effective-
ness of the measure over the long term. Dental
practitioners usually support fluoridation
because it is the right thing to do, even though
some have had reservations about diminished

practice income as a result. People opposed to
fluoridation may claim that “costs” include
social costs such as alleged ill health and envi-
ronmental damage. An economic analysis of
water fluoridation, under modern conditions of
widespread availability of fluorides, found that
under typical conditions the annual per person
cost savings in fluoridated communities ranged
from $15.95 in small communities (fewer than
5000) to nearly $18.62 in larger communities
(more than 20,000). This analysis took into
account the costs of installing and maintaining
necessary equipment and operating water
plants, the expected effectiveness of fluorida-
tion, estimates of expected cavities in nonfluori-
dated communities, cost of treatment of
cavities, and time lost visiting the dentist for
treatment.62
A 1989 workshop found that per capita cost
was affected by the following:
●
The size of the community: the bigger the
population to be reached, the lower the per
capita cost
●
The number of F injection points required
in the water system
●
The amount and type of equipment used
●
The amount and type of F chemical used,
its price, and the cost of transportation and
storage
●
Probably the expertise of water plant per-
sonnel99
Although city managers may well be im-
pressed by the low per capita cost, they will be
more immediately interested in the total front-
end expenditures. This information will best
come from the state health department’s water
supply division, because each community has
its own characteristics. The CDC can also help.
Per capita cost is generally inversely propor-
tional to the size of the population to be served,
although total expenditures on equipment
and material are naturally greater in larger
communities.
F compounds used in fluoridation are
sodium fluoride and sodium silicofluoride,
both solids, and hydrofluosilicic acid, a liquid.
The availability, and hence price, of all three is
highly variable, and prices can also be greatly
affected by fluctuations in transportation costs.
If a water system has several sources, such as a
river plus a number of wells, a separate set of
fluoridation equipment may be required for
25 Fluoridation of Drinking Water 339
each. Where natural F content is relatively high,
less F needs to be added, which thus reduces the
cost of supplies.
Although additional personnel costs for
fluoridation at a water treatment plant are virtu-
ally negligible in a large city, they can be a
significant factor in the running costs of fluori-
dation in a small community. The CDC recom-
mends that water plant operators receive at least
1 day/year of training to allow them to remain
efficient and up-to-date. This training may be
provided through the CDC’s technical assis-
tance program or may be given by health
department water supply personnel or univer-
sity faculty.
Savings in Treatment Costs
Data have been available for years to show that
the costs of restorative care for children
are sharply reduced by fluoridation. In the
Newburgh-Kingston study, initial dental care
for 6-year-old children cost 58% less in fluo-
ridated Newburgh than in nonfluoridated
Kingston.3 These savings came from the reduc-
tion in the number of extractions and restora-
tions needed, and the smaller proportion of
complex restorations required. Comparable
findings in British studies, which reported a sav-
ings of 49% for children ages 4-5 and 54% for
children ages 11-12, have been maintained even
after the caries decline was recognized.7
Some caveats are required, however, in inter-
preting these findings on cost savings. First,
whereas restorative costs for children are cer-
tainly decreased, the effect of fluoridation on
the costs of adult dental care is less clear. It
could be hypothesized, for example, that dollar
savings achieved early in life are lost in later life,
because greater tooth retention increases the
need for periodontal treatment and the place-
ment of crowns and bridges in later years. The
greater the degree of tooth retention, the more
dental services may be needed in the later years
of life. (Of course, this argument applies to
monetary expenditures only: the worth of a
healthy dentition throughout life will vary from
one individual to another—virtually beyond
price for some, of little value to others.)
A second caveat concerns the provision of
diagnostic and preventive services to children in
a fluoridated area. If many of these services are
only marginally necessary, supplying them will
340 The Distribution of Oral Diseases and Conditions
add to the cost of services without providing
much in the way of benefits. With declining
caries and the associated diminished need for
restorations, diagnosis and prevention assume a
greater proportion of the total cost of dental
care. Children with an obviously low caries
attack rate in a fluoridated area do not need to
visit the dentist as often as they used to, and
they require bitewing radiographs less fre-
quently. Data have also shown that F gel appli-
cations in an insured population, most of
whom lived in a fluoridated area, bore no rela-
tion to caries experience.37 If dentists continue
to see such children twice a year and apply the
full battery of diagnostic and preventive services
each time (all in the name of “good preventive
dentistry”), the substantial savings that can be
realized in the cost of restorative treatment will
be drastically reduced.18
POLITICS OF FLUORIDATION
Despite the powerful evidence in favor of water
fluoridation as public policy, its implementa-
tion has been sporadic in the United States and
even slower in most other countries. Frequently
it has been the subject of vigorous opposition.
Although the major arguments of opponents
have varied down the years, opposition remains
a persistent fact of life.
Whose job is it to see that fluoridation is
implemented in a community in which the con-
ditions are right for it? The ultimate decision is
made by mayors, town councils, state legisla-
tures, or the electorate. But these decisions do
not just happen by themselves. Dental profes-
sionals must make the main commitment to
promoting fluoridation, for without their sup-
port the issue will almost certainly fail.
However, the inherent problem is that this com-
mitment can demand a kind of leadership with
which dental professionals are often not com-
fortable: political action, public speaking, and a
level of visibility that can have troubling ethical
undertones. Dental and dental hygiene schools
do not train their graduates for political action.
The detailed role of dental professionals in pro-
moting fluoridation is discussed in Chapter 5.
Public Attitudes and Knowledge
Polls of public opinion down the years have
shown that the majority of Americans support
water fluoridation; opposition to fluoridation is
reported by 10%-20% of the U.S. population.
For example, a national Gallup poll in 1991
found that 78% approved of fluoridation,
although the sample was confined to parents.92
The 1990 National Health Interview Survey
found that 76% of those with more than 12
years of education knew what water fluorida-
tion was for, compared to 36% of those with
less than 12 years of education.56 Approval rat-
ings vary considerably in different regions and
communities, often according to whether fluor-
idation has been a recent local issue or not.
Although national and local studies find that
opponents of fluoridation constitute a minor-
ity,49 history has shown repeatedly that even a
small single-issue group, when dedicated and
well organized, can sway political decisions.
Many of those who say they are in favor are
really passively so, and a sizable proportion of
people polled in public opinion surveys are just
not particularly interested in fluoridation one
way or the other. This factor immediately evens
out the numbers in most political campaigns.
Social scientists were first attracted to the
fluoridation issue because of the community
conflict it generated, and much of their research
dates from the 1960s. Since then the volume of
social science research has diminished. That is
to be regretted, for common sense tells us that
some issues that dictate today’s attitudes toward
fluoridation, such as environmental concerns,
must have changed since the 1960s.
Some of this social science research attempted
to “profile” antifluoridationists, the rationale
being that opposition could then be predicted
and countered during promotional efforts.
Unfortunately, the infinite complexities of
human beliefs and behavior resulted in a picture
that is anything but clear. Some of the studies on
the attitudes of persons who voted against fluori-
dation in referenda, for example, concluded that
opponents felt a sense of deprivation or power-
lessness, and that they held a grudge against
“them,” the people whom they saw to be direct-
ing society. In this view, a general discontent with
society at large can be conveniently expressed by
opposing fluoridation.59,63,96,110
Although opponents of fluoridation have
been characterized as more likely to be older,
childless people of lower than median income
and education, a referendum can also fail in a

young, high-income, and highly educated com-
munity.109 The prevailing image of the profluo-
ridationist from the 1960s research is one of a
younger married person with small children
and with above-median income and education.
Even at that time, however, this image was
blurred by a finding of support in all SES
groups55 and by a Californian study that found
greater opposition to fluoridation among non-
manual than among manual workers.63
This confused picture of attitudes to fluori-
dation still pertained in more recent times.
A study in Norway, where there is no water
fluoridation, found a 20% rise in public oppo-
sition to fluoridated water between 1973 and
1983. Pinpointing the cause was difficult, but it
was thought to stem from a perception that
dental health was improving anyway so that
fluoridation was an unnecessary risk.102 In a
Massachusetts study 60% of the state’s voters
said they favored fluoridation in a telephone
survey, but this figure was at odds with the fact
that 61% voted against it in a referendum.129
Some have always opposed fluoridation on
the basis of freedom of choice71; that is, they
believe that the dichotomous nature of fluori-
dation (the community either fluoridates its
water or it does not) removes individual choice.
This issue remains alive and well, as some
would argue it should in a healthy society.
However one looks at it, the evidence is that
public attitudes toward fluoridating water have
become more accepting since opinions were
first measured in the 1950s.
Opposition to Fluoridation
The dichotomous nature of fluoridation ensures
that there will be organized political opposition
to its adoption. Even apart from specific argu-
ments on effectiveness and health effects, skilled
opponents can easily exploit the issues of “over-
regulation,” increasing environmental sensitiv-
ity, and cynicism about governmental policies
and officials.
Tactics of those opposed to fluoridation have
become more sophisticated in recent years.
Opponents, though small in number, have
learned how to exploit society’s concerns about
health, whether real or imagined, and how to
work effectively with legislatures and city coun-
cils. Most states have small “pure water coun-
cils,” loosely affiliated with each other, which
25 Fluoridation of Drinking Water 341
spring to life to oppose fluoridation when the
question arises in a community. There is also a
handful of PhDs, physicians, and dentists, who
tend to appear anywhere in the country (or in
the world, for that matter) to support a local
antifluoridation group.
Court Decisions on Fluoridation
Many communities that have begun water
fluoridation have had legal suits brought
against them in an effort to stop it. Although
lower courts have ruled against fluoridation in a
few of these many suits, fluoridation has never
been ruled against in appellate court. Lower
courts that have found against fluoridation have
usually done so on the basis of personal liberty
and religious beliefs.14,23,118
By as early as 1965 state supreme courts had
upheld the legality and constitutionality of
fluoridation on 13 occasions.103 By 1984, 13
appeals had reached the U.S. Supreme Court,
which on every occasion either dismissed the
appeal or refused review.14 No American court
of last resort has ever ruled against fluoridation
for any reason.
The most searching courtroom scrutiny of
water fluoridation, especially with respect to its
impact on human health, occurred in Glasgow,
Scotland, in 1983. Known as the Strathclyde
case, it was the longest court case in British legal
history. The presiding judge, Lord Jauncey, ruled
that the evidence for the safety of fluoridation
was convincing.87
Fluoridation Decisions at the Community
Level
Unless state law dictates otherwise, a decision to
fluoridate is made by the local entity under
whose jurisdiction the water supply falls. This
can be a city council, county commission, water
board, or board of health. Even when a city pro-
vides water to suburban areas and surrounding
townships, the decision remains that of the city
council, although the issue becomes more com-
plicated in these cases. In locations where the
issue is volatile, however, many councils do not
want to make the decision without a clear indi-
cation of public feeling, and that often means
holding a referendum.
The first referendum on fluoridation was
in 1950, in Stevens Point, Wisconsin.88 It
lost. McNeil’s entertaining description of that
342 The Distribution of Oral Diseases and Conditions
campaign shows how quickly fluoridation can
flare up into a major issue and how an unpre-
pared dental community, no matter how well
intentioned, can make some serious political
errors. The outcomes of referenda had not
improved much until recent times. It was esti-
mated in 1970 that two-thirds of the first 900
referenda were lost,76 and 33 of the 41 held in
1980 were also lost.48 The CDC records show
that in 2000-03 referenda were successful 58%
of the time, and in cities with more than
150,000 people the figure was closer to 75%.
This improvement tells us that dentistry is
learning how to act in these situations and that
perhaps the idea of fluoridation is not as con-
tentious as it once was in the national con-
sciousness. Perhaps we can even say that water
fluoridation has become institutionalized.
THE FUTURE
Chapters 24 and 25 have examined the F issue
from many perspectives. It all began with
Colorado brown stain and it led to water fluori-
dation, dentistry’s greatest contribution to the
public’s health. F has changed the face of
America (literally!), banished childhood tooth-
ache for millions, and raised the prospects of an
uneventful lifetime dental history for millions
more. Its controlled use has improved the qual-
ity of life for all it reaches, and good oral health
is primarily a quality-of-life issue. It is the most
cost-effective method of bringing F to a commu-
nity, and it benefits the socially deprived rela-
tively more than the socially advantaged. F has
also probably done more to change the nature
of dental practice over the last generation than
any other single factor.
Despite all those benefits, and despite the
fact that fluoridation reaches over 62% of the
American population, recent progress has been
slow. Society changes and issues that were not
considered during the time of Dean and
McClure nor during the 1950s and 1960s
when steady progress was made in implement-
ing fluoridation have to be dealt with if
progress is to continue. Social science research
on public acceptance of fluoridation has not
moved forward much since the 1960s, and
some feel that dental, medical, and social
researchers have at least partly failed to carry
on from the superb start that the Dean-
McClure generation gave us. Proponents of
fluoridation have also made honest mistakes
in promoting it. What appeared to some, in
retrospect, as arrogance and complacency in
past years can still present problems in pro-
moting fluoridation today. In a free society,
water fluoridation can only continue as public
policy if the public accepts it.
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 26 Other Uses of Fluoride in Caries
Prevention
FLUORIDATED SALT
FLUORIDATED SCHOOL DRINKING WATER
FLUORIDATED MILK
DIETARY FLUORIDE SUPPLEMENTS
Caries Prevention by Fluoride
Supplementation
Dosing Schedules
Fluorosis Risk from Fluoride
Supplementation
Appropriate Use of Fluoride Supplements
Prenatal Fluoride Supplementation
Fluoride (F) was first used to prevent dental
caries by adding it to drinking water, but it was
not long before alternative methods were put
into practice. The result today is that F is used
in a variety of ways to control caries in public
health programs, individual patient care, and
self-care. Dental professionals today must use
F with the knowledge that there is extensive
background exposure to F through drinking
water, toothpaste, mouthrinses, and processed
food and drink. We stated in Chapter 24 that
F works best to control caries when low ambi-
ent levels are constantly present in the oral
cavity (in plaque, saliva, enamel surface, soft
tissues). Any use of F rinses, professionally
applied gels, or F dietary supplements should
be aimed toward achieving that condition,
either for the individual patient or for the
public.
This chapter examines the evidence to sup-
port the use of F in salt, school drinking water,
milk, dietary supplements, professionally
applied gels and varnishes, and F mouthrinses,
and makes recommendations for their use. The
chapter closes with an assessment of multiple
F exposures.
PROFESSIONALLY APPLIED FLUORIDE
GELS
FLUORIDE VARNISHES
FLUORIDE MOUTHRINSES
FLUORIDE TOOTHPASTES
Quality of the Fluoride Toothpaste Trials
Fluoride Concentrations in Toothpastes
Standards for Toothpaste Efficacy
Global Impact of Fluoride Toothpastes
MULTIPLE FLUORIDE EXPOSURES
FLUORIDATED SALT
Salt fluoridation is the controlled addition of
F to domestic salt (F salt) for the purpose of pre-
venting dental caries. Salt fluoridation follows
the same public health principle as water fluori-
dation: namely, that a small amount of F in a
dietary staple serves to inhibit dental caries with
little conscious action on the individual’s part.
The concept of adding F to salt followed the suc-
cess of iodization of salt, which had been initi-
ated in Switzerland in 1922 to prevent goiter,
the thyroid condition endemic to the Swiss
Alpine region at the time.
F salt was first used in Switzerland in 1955.
There is no water fluoridation in Switzerland,
and the nation has only one salt processing and
distribution company. Switzerland is a prosper-
ous, highly developed country, and there have
been few problems with safety and control of
the procedure. The reduction in caries incidence
in Swiss communities in which F salt has a good
market share, although measured only in
before-after designs, appears similar to that
found with water fluoridation.38,110,146 F salt
has been well accepted by the Swiss public and
347
348 Prevention of Oral Diseases in Public Health
now accounts for approximately 80% of the salt
market. The effects of salt fluoridation have also
been studied in Colombia65 and Hungary150
with generally favorable results, and good
results have been reported in Jamaica58,112 and
Mexico.81 Worldwide, it is estimated that
approximately 40 million people consume F
salt daily.125
Although the evidence for the effectiveness
of F salt is consistent, it comes from only a lim-
ited number of observational studies rather
than from clinical trials. The results of the
observational studies have been contaminated
by the concurrent use of F toothpaste, so that
not all of the observed reduction in caries can
be attributed to consumption of F salt.165 In
terms of how F salt works to inhibit caries, sali-
vary F concentration has been found to show
a small but significant increase for at least
5 minutes after ingestion of the F salt, and these
levels return to baseline in 20 minutes.103 Given
the role of salivary F as a reservoir (see Chapter
24), this appears to be how F salt produces its
beneficial effects.
The concentration of F in salt is based on
estimates of salt consumption and is evaluated
by studies of urinary F concentration. The
material most commonly used to fluoridate
salt is potassium fluoride (KF), although
sodium fluoride (NaF) is also used. The early
Swiss studies began with salt fluoridated to 90
parts per million (ppm), but it soon became
clear that this level was too low. In the early
1970s the concentration was increased to
250 mg KF/kg salt (or 225 mg NaF/kg salt), a
level based on estimated adult salt consump-
tion of some 8-10 g/day. Although patterns of
salt consumption vary from one country to
another,80 250 or 350 mg KF/kg salt now
appears to be the standard in Switzerland and
other countries as well.
Salt fluoridation has political appeal because
it gives consumers a choice in a way that water
fluoridation does not. In most places using
F salt, it appears alongside nonfluoridated salt
on the supermarket shelves, and purchasers can
make their own choices. The Swiss canton of
Vaud, interestingly enough, removes that choice
by fluoridating all salt available on the super-
market shelves as well as the salt delivered in
bulk to restaurants, bakeries, food processors,
hospitals, and other institutions. Oral health
should benefit as a result, although consumer
choice is curtailed.
Some concerns have been expressed that
use of F salt may promote increased salt con-
sumption with possibly detrimental effects on
hypertension, although there is no evidence
that this has happened. Nothing in the use of
F salt encourages people to consume more salt
than usual.
By the mid-1990s use of F salt was established
in France, Germany, Belgium, Spain, and the
Czech Republic, as well as in Switzerland. In
Switzerland the market share is around 80%,
and in Germany it is over 60%. In the western
hemisphere, F salt use is established in 14 coun-
tries of South America and the Caribbean, most
notably Costa Rica, Mexico, Colombia, Ecuador,
Uruguay, Venezuela, and Jamaica. Further
growth in Latin America is planned. F salt has
never been used in the United States or Canada,
and given the mass distribution of food, the
multiple salt production companies, and the
extent of water fluoridation, salt fluoridation
would not be appropriate in either country.
FLUORIDATED SCHOOL DRINKING
WATER
In rural areas in which community water fluor-
idation is not possible, the approach of
fluoridating the schools’ drinking water was
promoted for some years. The procedure was
reported to reduce dental caries among school-
children by about 40%,75 although none of
these studies was conducted blind and there
were no concurrent controls.
Relative to community water fluoridation,
the disadvantages of school water fluoridation
are that children do not receive the benefits
until they are old enough to begin school, and
of course they drink the water only when school
is in session. To compensate for this reduced
exposure, the recommended concentration is
4.5 times the optimum for community-wide
water fluoridation. At its peak, school water
fluoridation was introduced in 13 states in the
United States. Data reported by states to the
Division of Oral Health of the Centers for
Disease Control and Prevention (CDC) show
that in 1981 school water fluoridation was
established in 470 schools serving some
170,000 children. Its current extent is not

known but is much lower than the 1981 peak.
There is no record of the procedure’s being used
in countries outside the United States.
Despite the CDC’s issuance of safety guide-
lines, a number of overspill mishaps have
occurred, fortunately without lasting ill
effects.3,72,163 The CDC no longer promotes
school water fluoridation.
FLUORIDATED MILK
Milk fluoridation is the addition of a measured
quantity of F to bottled or packaged milk
(F milk) to be drunk by children. The rationale
is that this procedure targets F directly to chil-
dren, and thus it should theoretically be more
efficient than fluoridating the drinking water.
Having both fluoridated and nonfluoridated
milk available also maintains consumer choice.
The mode of action seems to be from salivary
return of F to the oral cavity.160 Salivary F levels
are raised 45 minutes after ingestion,26 and
plaque F levels are raised threefold over resting
levels for up to 4 hours after ingestion.57,126
Urinary F levels in children are similar to those
found in a community with water fluoridated
at 1 ppm.88
Only one randomized double-blind trial has
been conducted to test the efficacy of consump-
tion of F milk,147 although a test of F milk read-
ily fits the randomized design. Other studies
examining the efficacy of milk fluoridation
have been seriously flawed. A few public health
programs using fluoridated milk have become
established, such as in Bulgaria119 and in St.
Helens, near Liverpool.97 However, it is hard to
recommend further research into milk fluorida-
tion for the United States in view of the large
number of F vehicles available today.
DIETARY FLUORIDE SUPPLEMENTS
Because the assumption in the 1940s was that
the effect of fluoridated water was mainly
preeruptive, dietary supplements were intended
to mimic the observed action of fluoridated
water. F supplements in the form of tablets,
lozenges, drops, liquids, and F-vitamin prepara-
tions have been used around the world since
the 1940s.
F supplements have F quantities of 1 mg,
0.5 mg, or 0.25 mg. They were originally made
26 Other Uses of Fluoride in Caries Prevention 349
as a 1-mg F pill to be dissolved in a liter of the
infant’s drinking water, an approach which in
time gave way to the simpler once-a-day inges-
tion of the tablet. Later, chewable tablets and
lozenges were manufactured for older children,
to be chewed or sucked 1-2 minutes before
swallowing, the intent here being to obtain
both topical and systemic effects. Most tablets
contain neutral NaF, although acidulated phos-
phate F (APF) tablets have been tested. There
are also F-vitamin drops for infants, often
prescribed by pediatricians.
Caries Prevention by Fluoride
Supplementation
Early studies of the preeruptive caries-preven-
tive effects of F supplementation in children
were often seriously deficient and thus yielded
questionable results. Some of the highest caries
reductions, around 80% over several years, were
reported by American studies in the mid-
1970s,1,105 but flaws in these studies included
self-selection into test and control groups or the
absence of concurrent controls, high attrition
rates, and nonblinded examiners. The associa-
tion that practitioners have observed between
conscientious use of F supplements and free-
dom from caries also cannot be taken as evi-
dence of efficacy, because compliance with the
F supplementation regimen is naturally higher
among dentally aware people who also have
other good oral health habits.
Evidence to favor a preeruptive benefit from
F supplementation remains limited to retro-
spective analyses. Positive results have been
reported retrospectively,5,32,40,41,60,108,166,167
but self-selection bias was evident in all of these
studies. Other retrospective studies found no
difference in caries experience between those
children who reported using F supplements and
those who did not.14,17,64,74,86,155
Although the evidence for preeruptive
benefits from F supplementation is weak, well-
conducted randomized clinical trials using
placebos and blinded examiners have shown
that it can have posteruptive benefits in school-
age children. Studies in which the supplements
were chewed, swished, and swallowed under
supervision have reported caries reductions of
20%-28% over 3-6 years.43,50 Caries reductions
of 81% were reported in a Glasgow study in
which children from lower socioeconomic
350 Prevention of Oral Diseases in Public Health
groups who were initially 5.5 years of age
sucked a 1-mg F tablet or a placebo under super-
vision in schools every school day for 3 years.148
In summary, F supplements have a posterup-
tive effect because they meet the goal of main-
taining ambient F in the oral cavity. However,
there is no good evidence to demonstrate a
preeruptive benefit.
Dosing Schedules
To obtain F supplements in the United States
and Canada, a prescription by a dentist or
physician is required; both the American Dental
Association (ADA) and the American Academy
of Pediatrics (AAP) maintain schedules of rec-
ommended doses of F supplements. However,
before 1979 the two schedules did not coincide:
the AAP first recommended 0.5 mg/day6 for
children under 2 years of age, whereas the ADA
recommended 0.25 mg/day. The AAP altered its
earlier recommendations7 in 1979 to bring
them into line with those of the ADA and reaf-
firmed these new recommendations in 1986.8
As the dosing schedules for F supplements are
revised periodically, the trend has been to make
them ever more conservative. In response to the
growing evidence that use of F supplements is a
risk factor for fluorosis, the ADA revised its
schedule in 1994 to reduce the amount of
F ingested by young children, and the AAP
accepted this schedule a year later.9 The current
ADA-recommended schedule, based on the
age of the child and the concentration of F in
the water supply, is shown in Table 26-1. The
thinking in Europe is similarly conservative: a
European Community group recommended that
a supplement of 0.5 mg F be used only for “at-
risk” individuals from the age of 3 years onward.
This group also declared that F supplementation
had no place as a public health measure.34
Table 26-1 Recommended dosage levels of
supplemental fluoride as established by the American
Dental Association in 1994 (in mg F/day)12
Concentration of Fluoride in Water (ppm)
Age <0.3 0.3-0.7 >0.7
6 mo–3 yr 0.25 — —
3-6 yr 0.50 0.25 —
6-16 yr 1.00 0.50 —
Fluorosis Risk From Fluoride
Supplementation
Reduction of the early AAP recommendation of
0.5 mg/day for children under 2 years of age was
overdue, for this dosage probably led to a con-
siderable degree of fluorosis. One study in the
Boston area that used the old AAP schedule, for
example, was successful in terms of caries reduc-
tion, but 67% of the children developed very
mild or mild fluorosis.2 Excess F ingestion in
infancy and early childhood through inappro-
priate prescription of F supplements is unfortu-
nately more common than it should be. A 1980
national survey of pediatricians found that
around 20% of them who practiced in fluori-
dated areas were prescribing F supplements for
child patients who lived in the same communi-
ties,104 a clearly inappropriate action that
increases the risk of dental fluorosis. Things
were no better 15 years later.124 These studies
have emphasized the need for continuing edu-
cation of both physicians and dentists. If sup-
plements are to be prescribed at all, they should
certainly not be prescribed for patients who
consume fluoridated water.
The major concern now associated with sup-
plement use is that of dental fluorosis.
Although fluorosis can develop at any preerup-
tive stage, late secretion and early maturation
have been identified as the developmental
times when dental enamel is especially sensitive
to ingested F.42,59,95 Although some studies
found no association between supplement use
and the development of fluorosis,15,171 con-
siderably more have reported a clear associa-
tion.2,39-41,74,86,94,96,133,153,155,169,170 A series of
excellent case-control studies has provided
strong evidence for a cause-and-effect relation
between use of F supplements and dental fluo-
rosis,121-123 and a comprehensive meta-analysis
also concluded that use of F supplements is a
risk factor for fluorosis.83
The weight of evidence is that F supplements,
when ingested prior to tooth eruption, are a risk
factor for dental fluorosis in both fluoridated
and nonfluoridated areas.
Appropriate Use of Fluoride
Supplements
Although F supplements are reportedly used by
some 16% of American children under 2 years

of age,117 their continued prescription in North
America needs to be thoughtfully reviewed. As
often is the case in public health, their use
requires trade-off decisions: F supplements have
some beneficial impact on oral health, but there
is also the hazard of fluorosis when they are
used in an era of wide exposure to F. The reasons
why prescription of F supplements for infants
and young children needs to be considered
carefully can be spelled out as follows:
●
Evidence to support a preeruptive anticari-
ogenic effect for F supplementation is
weak.
●
F supplementation has been identified as a
risk factor for dental fluorosis, and the
prevalence of fluorosis is increasing.
●
The prevalence of caries continues to
decline, which reduces the need to pursue a
strategy that carries documented risks with
little counterbalancing benefit.30
In light of the advantages and disadvantages
of F supplements in a time of widespread
F exposure, calls have been made for a reevalua-
tion of their use among young children.14,82,132
They have a place when used to achieve a
posteruptive effect in children older than
7 years, and it is likely that they would be useful
in the growing population of older dentate peo-
ple who are at risk of both coronal and root
caries, although this issue has not yet been stud-
ied. At the very least, when F supplements are
prescribed for infants and young children,
parents or guardians should be informed of the
fluorosis risk that accompanies the limited car-
iostatic benefits.
Prenatal Fluoride Supplementation
The question of whether to prescribe F supple-
ments for an expectant woman to increase
caries resistance in the offspring has been
debated for years. In light of the discussion on
dietary F supplements in general, it is not sur-
prising that current views are that any enhanced
resistance to caries will be only minor at best.
The only prospective randomized trial of prena-
tal F supplementation found no significant
difference in the caries experience of the off-
spring.100 Therefore use of prenatal supple-
ments is not recommended.
F can cross the placental barrier and enter the
fetal circulation.31,120 Fetal plasma F levels are
correlated with maternal levels, although gener-
26 Other Uses of Fluoride in Caries Prevention 351
ally they are lower. F is taken up in the mineral-
izing tissues of the fetus; fetal enamel levels
go up with an increase in maternal plasma F lev-
els.120 The most critical time for F uptake in
enamel, as noted earlier, is the late secretion
and early maturation phase. As a result, prenatal
F exposure will have little effect, especially since
mineralization of even primary teeth is not far
advanced at birth.
Collectively the research evidence suggests
that prenatal F administration cannot be sup-
ported. As long ago as 1966, the U.S. Food and
Drug Administration banned advertisements
which claimed that prenatal F administration
would increase the caries resistance of off-
spring.161 No convincing research has emerged
since then to change that picture, and hence the
ban still pertains. Although there is nothing to
suggest that prenatal F supplementation will
harm either fetus or mother, no evidence exists
to support claims of prenatal benefit.
PROFESSIONALLY APPLIED
FLUORIDE GELS
The F compounds that dental professionals rou-
tinely use in tray applications are highly con-
centrated, and careful attention to technique
and to the amounts used is required. Table 26-2
lists the quantities and concentrations of the
F compounds most frequently used in dental
practice, as well as those used in public health
programs and self-applied by individuals.
Box 26-1 is a guide to estimating the amounts
of F in dental products, and Box 26-2 brings
together the information on toxic exposure to F.
Early work on professionally applied F began
even before the first water fluoridation proj-
ects21,91 and within a few years the Knutson
technique was developed.90 In this method, a
2% solution of NaF is applied in a series of four
treatments over a period of several days, follow-
ing an initial prophylaxis. In the 1950s the
annual application of 8% stannous fluoride
(SnF2) was reported to give beneficial results
similar to those achieved with NaF. But staining
problems were reported, and the material had
an unpleasant taste. Since the early 1960s, APF
has become the most widely used F compound
for professional application. This material has a
pH of about 3.0 and was developed after experi-
mental work showed that the topical uptake of
352 Prevention of Oral Diseases in Public Health

Table 26-2 Concentration and quantity of fluoride in commonly used topical fluoride compounds
Compound Concentration (ppm) Quantity

Topically applied agents

2% NaF 9050 45 mg in 5 ml*
1.23% APF solution, gel, or prophylactic paste 12,300 62 mg in 5 g
8% SnF2 solution 19,363 97 mg in 5 ml
0.4% SnF2 gel 968 4.9 mg in 5 g
5% NaF varnish (2.26% F) 22,600 51 mg in 5 ml

Mouthrinses
0.2% NaF—weekly 905 9 mg in 10 ml†
0.05% NaF—daily 226 2 mg in 10 ml
0.1% SnF—daily 242 2 mg in 10 ml
APF rinse (0.1% fluoride)—weekly 1000 10 mg in 10 ml
APF rinse (0.022% fluoride)—daily 200 2 mg in 10 ml
1 mg in 5 ml of oral rinse supplement
(rinse and swallow)

Toothpastes
0.76% Na2 FPO3 1000 1 mg/g‡
0.243% NaF 1105 1.1 mg/g
1.14% NaF 1500 1.5 mg/g
0.4% NaF 966 1 mg/g
0.4% Na2 FPO3 526 0.5 mg/g
0.304% Na2 FPO3 401 0.4 mg/g
Note: Some figures are rounded.
APF, Acidulated phosphate fluoride.
*A topical application or prophylactic treatment uses about 5 ml or 5 g of material.
†Amounts of 5 and 10 ml are used in supervised mouthrinsing.
‡An average load of toothpaste on the brush is about 1 g.

F by enamel was greater in an acidic environ-
ment.28 The agent has been tested in several
concentrations, the most common being 1.23%
F, usually as NaF, in orthophosphoric acid. The
material is nonirritating and nonstaining, will
tolerate the addition of flavorings, and is well
accepted by patients.
Procedures for the professional application
of F agents were originally developed on the
assumption that the F would form a fluorapatite
in the crystalline structure of the enamel. A
prophylactic treatment was thus considered
mandatory before the application of the F to
maximize this reaction. Subsequent research,
however, shows that high-concentration F such
as that in APF gels tends to form a “calcium flu-
oride–like” material on the enamel surface46
and thus serves as a reservoir of F that becomes
available for remineralization when pH drops.
The nature of this calcium fluoride–like mate-
rial is still debated by scientists, but as a result of
its formation, a prophylaxis before a profes-
sional F application is unnecessary because it is
no more beneficial than toothbrushing and
flossing by the patient.79,134,137 This finding
allows a considerable time savings in office F
applications. Professional gel-tray applications
have long been considered not to be cost effec-
tive for public health programs, although they
might be a reasonable approach for highly sus-
ceptible special groups in targeted programs.99
F-containing prophylactic pastes are widely
used in dentistry; the reasoning behind their
development was that the prophylaxis and
the professional F application could be carried
out at the same time. However, results from
clinical trials that tested this procedure were
disappointing. When a prophylactic paste is to
 26 Other Uses of Fluoride in Caries Prevention 353

BOX 26-1 How To Estimate the Amount of Fluoride in a Dental Product

Basic information

1 oz = 28.4 g

“Percent” means g or ml per 100 g or ml; e.g., 2% NaF solution means 2 g NaF per 100 ml water

Atomic weights: Na = 23; F = 19, Sn = 119; P = 31; O = 16

Fluoride compounds most often used are NaF, SnF2, Na2FPO3

Example 1: How much F is in 10 ml of 0.05% NaF mouthrinse?

The mouthrinse has 0.05 g of NaF per 100 ml of rinse

= 50 mg of NaF, or 5 mg of NaF per 10 ml

Amount of F = 5 × 19/42 = 2.26 mg

Example 2: How much F is in a 6.4-oz tube of Colgate MFP toothpaste? (6.4 oz = 181.8 g)

Colgate with sodium monofluorophosphate (MFP) is 0.76% Na2FPO3, so it has 0.76 g of MFP per 100 ml of
toothpaste

Grams of Na2FPO3 in a 6.4-oz tube = 0.76 × 181.8/100 = 1.38 g, which is 1380 mg Na2FPO3

Amount of F in the tube = 1380 × 19/144 = 182.1 mg

Example 3: How much F is in an 8.2-oz tube of Crest toothpaste? (8.2 oz = 232.9 g)

Crest contains 0.243% NaF, so it has 0.243 g of NaF per 100 ml of toothpaste

Grams of NaF in an 8.2-oz tube = 0.243 × 232.9/100 = 0.566 g, which is 566 mg NaF

Amount of F in the tube = 566 × 19/42 = 256 mg

BOX 26-2 Data on Toxic Fluoride Intake Levels in Humans29,69

●
Certainly lethal dose (CLD) = 32-64 mg F/kg body weight.
●
Death is likely in a child who ingests more than 15 mg F/kg body weight.
●
Probably toxic dose (PTD), defined as the minimum dose that could cause toxic signs and symptoms, including
death, and the ingestion of which should trigger immediate intervention and hospitalization = 5 mg F/kg body
weight.
The 10th and 90th percentiles of weight for children at various ages are as follows:
Age Weight
1 year 8-12 kg
2 years 10-15 kg
3 years 12-17 kg
4 years 14-20 kg
6 years 17-27 kg
8 years 22-34 kg
So for a child about 7 years of age, who would weight approximately 20 kg, the PTD would be around 100 mg F.
354 Prevention of Oral Diseases in Public Health
be used it should routinely be an F-containing
paste, but such use is not by itself a substitute
for a professional F gel application.
FLUORIDE VARNISHES
F varnish is not intended to be as permanent as
a fissure sealant (see Chapter 27); rather it is a
vehicle for holding F in close contact with the
tooth for a period of time. A theoretical advan-
tage for varnishes over other methods of pro-
fessional F application is that varnishes are
adhesive and hence should maximize F contact
with the tooth surface. Varnishes are a way of
using high F concentrations in small amounts
of material. F varnishes are widely used in
Europe and Canada, and were accepted for use
in the United States in 1994.
Early European clinical trials on the efficacy
of F varnishes gave mixed results,73,93,116 and a
large clinical trial in Quebec, which ran for
nearly 5 years in communities chosen for their
high caries experience, reported only moderate
efficacy.33 As with most modern clinical trials in
North America, the study was conducted in an
environment of extensive F exposure from
toothpaste, which always makes the impact of
any one F vehicle difficult to discern. Later stud-
ies in Europe demonstrated the efficacy of F var-
nishes.37,71 They have been shown to slow the
progression of existing enamel lesions127 and to
be at least as effective as APF gel when applied
semiannually.142 A systematic review found
that there was a substantial caries-preventive
effect from F varnishes, although this conclu-
sion was based mostly on studies that used no
concurrent controls.106
Varnishes must be reapplied at regular
intervals to maintain their cariostatic effect,141
and investigations continue into the optimum
application frequency. Varnishes are clearly
effective, although as a professionally applied
agent they are inherently more expensive than
self-applied preventives. It is not yet clear
whether varnishes can be most efficiently used
in clinical programs in high-caries popula-
tions or whether their use is best reserved for
treatment of individual patients on an ad hoc
basis. In any event, they are a useful addition
to the dental practitioner’s F armamentarium
for use in caries-susceptible patients. They
have, for example, been found effective in pre-
venting decalcification beneath orthodontic
bands.4
Several interesting public health programs
in the United States use F varnish to bridge the
gap between dental and medical practice. One
program is working to bring appropriate use
of F varnish into the medical school curricu-
lum,66 whereas in another, physicians in most
of North Carolina use F varnish to prevent
early childhood caries in their at-risk young
patients.139 This latter program is premised on
the fact that a much higher proportion of
infants visit a physician’s office than visit a
dental office (see Chapter 2). Contrary to
some expectations, the physicians and their
staff have reacted positively, which offers
exciting prospects for the prevention of this
distressing condition, as well as closer cooper-
ation between the professions.
FLUORIDE MOUTHRINSES
The idea of preventing caries by rinsing the
mouth with dilute F solutions has been around
for decades,21 but it was some years before
F mouthrinsing became a standard procedure in
preventive dentistry. A Swedish report in 1965
that found a nearly 50% reduction in caries
increment over 2 years157 naturally sparked
interest in the procedure. Since then, NaF rinses
have been extensively tested; other rinses tested
to a lesser extent include those containing APF,
SnF2, ammonium fluoride, and amine fluoride.
NaF rinses became the most widely used of
these products because of lower expense and
better taste.
NaF formulations have been tested as a
weekly rinse at 0.2% F and as a daily rinse at
0.05% F. School-based programs have found
the weekly regimen to be the most convenient,
whereas daily rinsing is most appropriate for
individual use. The caries reductions from daily
rinsing are only slightly greater than those from
weekly rinsing,52,70 and the slight differences do
not compensate for the greater practicality and
lower cost of weekly rinsing in a school-based
program. For home use, dentists can advise
patients to buy an F mouthrinse from the drug-
store or supermarket. Products come and go;
a list of current products with ADA approval can
be found on the ADA’s website (http://www.
ada.org/ada/seal/sealsrch.asp).

Most studies testing the efficacy of NaF rinses
date from the 1970s. Collectively they showed
that regular use of NaF mouthrinses reduces
caries increments in children by 20%-35% over
periods of 2-3 years.23,44,63,76,136,140 Positive
benefits were also reported in the primary den-
tition.136 APF rinse-and-swallow rinse is also
beneficial,1 although given the potential for flu-
orosis from systemic absorption, this product
should be prescribed with caution in younger
children. A limited number of tests with 0.1%
SnF2 rinse have demonstrated positive caries
reductions,111,128 and SnF2 has also demon-
strated antibacterial properties not possessed by
NaF.154,156 Continuing caries reductions over
long-term use of 10 years or so were reported,22
and retained benefits have also been found in
children some years after they completed a
school rinsing program.67,98
F mouthrinsing became established as a
major caries-preventive public health program
in the United States, Canada, and other coun-
tries during the 1970s. According to the CDC,
3.25 million American schoolchildren were in F
mouthrinsing programs in 1988, spread over
11,000 sites. This number has dropped consid-
erably since then because cost effectiveness
is hard to maintain with declining caries levels.
Despite all these seemingly favorable results,
a systematic review found that there were not
enough high-quality trials from which to reach
a conclusion on the efficacy of F mouthrinses.16
However, it was the National Preventive
Dentistry Demonstration Program (NPDDP), a
large program conducted in 10 U.S. cities during
1976-81 to compare the costs and effectiveness
of a series of preventive mechanisms, that raised
most doubts about F mouthrinsing as a public
health procedure.
The NPDDP found that the effectiveness of
F mouthrinsing was poor, both in overall
results89 and in separate assessments of first-
grade children with high and low caries incre-
ments.48 Earlier reviews by the NPDDP
researchers had reported serious flaws in the
conduct of many earlier studies that did not use
concurrent control groups25 and in some of the
economic analyses that led to the assumption
of cost effectiveness.145 Quite strong criticism
was also leveled at the way in which the
National Institute of Dental and Craniofacial
Research had used its data to promote the use of
26 Other Uses of Fluoride in Caries Prevention 355
F mouthrinses in public health programs.47 At
the same time, the NPDDP itself was criticized
on the grounds of faulty design and analysis.61
The atmosphere of uncertainty was dissipated
to some extent at a workshop on the cost effec-
tiveness of preventive procedures in 1989,
where it was concluded that F mouthrinsing is a
reasonable procedure to use in high-risk indi-
viduals or groups, though of questionable cost
effectiveness as a population-based strategy.99
This debate emphasizes the need for clinical
trials to be conducted with due regard for
the principles of experimental studies (see
Chapter 13) and the dangers in extrapolating
data from demonstrations and other noncon-
trolled projects to public policy. F mouthrinsing
continues to be used in public health projects,
although program directors are taking more
care in the selection of communities in which to
conduct them: for example, such projects are no
longer promoted in fluoridated communities.
F mouthrinsing is now seen as appropriate for
high-risk groups rather than as a population
strategy.
FLUORIDE TOOTHPASTES
Toothpastes without active ingredients, mean-
ing those that contain abrasive and flavoring
agents only and thus are intended for oral
hygiene and cosmetic benefits, have no anti-
caries action by themselves. But because tooth-
brushing is a social norm in high-income
countries, a variety of preventive and thera-
peutic agents (both known and hypothetical)
have been added to toothpastes over the years.
Early efforts to produce anticariogenic tooth-
pastes included the addition of ammonia,
antibiotics, chlorophyll, and various other
agents to toothpastes. None of these agents was
effective. To date, F is the only nonprescription
toothpaste additive that has been shown to
prevent caries.
The earliest attempts to add F to toothpaste
were unsuccessful because of the incompatible
abrasives used in the products, which bound
the F and thus made it biologically unavailable.
The first successful clinical trials of an F additive
used SnF2 with a calcium pyrophosphate abra-
sive.115 These positive results were repli-
cated during the 1960s in other American and
British studies using the same formulation, and
356 Prevention of Oral Diseases in Public Health
caries reductions in children in the 15%-30%
range over 2-3 years were reported.77,84,85,114,144
Clinical trials of F toothpastes in fluori-
dated areas have demonstrated an additive
effect,101,109,164 and there is some evidence that
use of F toothpaste prevents root caries in older
adults.18
In all, more than 90 clinical trials have been
conducted with various F compounds as the
active ingredient: SnF2, NaF, sodium monofluo-
rophosphate (MFP), and amine fluoride have
all been successfully tested.35 Even more
compatible abrasives have been developed
and tried: insoluble metaphosphate, sodium
trimetaphosphate, hydrated silica gel, calcium
carbonate, dicalcium dihydrate, and calcium
pyrophosphate are the main ones. New formu-
lations are constantly under investigation and
are soon marketed when found effective.
There is some laboratory evidence that tooth-
pastes with NaF are more efficacious than those
with MFP, although clinical data on this subject
are hard to interpret. Analyses of data available in
the early 1990s were split on the issue, with dis-
cussion often becoming pedantic. Subsequent
clinical trials that gave a slight edge to NaF
required very large groups to show statistical sig-
nificance,107,149 and another trial found no dif-
ference between NaF and MFP products.45 Given
the size of the market, this sort of dueling is likely
to continue, although it seems unlikely that there
will be a serious difference between the products
at the population level.
Serious marketing of F toothpastes was
underway by the early 1970s, and public accept-
ance was immediate in virtually all of the high-
income nations. By the 1990s, F toothpastes
accounted for well over 90% of the toothpaste
market in the United States, Canada, and many
other countries. Their use in low-income coun-
tries, where F toothpastes could potentially fill
an important preventive role, is inhibited by
their relatively high cost and poor distribution,
and often by the relative absence of oral hygiene
methods that are taken for granted in the devel-
oped world. The FDI World Dental Federation
is looking for ways to develop affordable
F toothpastes (http://www.fdiworldental.org),
but progress is slow. The development of afford-
able F toothpaste for the low-income world is a
challenge to the manufacturers and to dentistry
in general.
Quality of the Fluoride Toothpaste Trials
It must be stated at this point that many of the
clinical trials for F toothpaste are among the
most elegant trials to be found in dentistry, or in
all of biomedicine for that matter, to demon-
strate the efficacy of a product. All of the essen-
tial features of the best clinical trials (see
Chapter 13) can be found in many of these
studies: randomized groups, double-blind
designs, placebo controls, meticulous proce-
dural protocols. Because the water fluoridation
field trials have inherent design limitations (see
Chapter 25), opponents of fluoridation can
attack their validity. But if the issue is the effi-
cacy of F exposure, the F toothpaste trials collec-
tively include many studies that meet the gold
standard for such trials. Taken together, the
toothpaste trials provide the strongest evidence
we have that F exposure is efficacious in control-
ling caries.
Fluoride Concentrations in Toothpastes
The F toothpastes that first became widely
marketed contained about 1000-1100 ppm F.
When introduced into the oral cavity, F in
toothpaste is taken up directly by demineral-
ized enamel,129,152 although its retention on
sound enamel is thought to be of relatively
minor importance. It also increases the F con-
centration in dental plaque,54,55,143 thus leav-
ing a store of F available for remineralization
when pH drops. Salivary F levels, normally low
in resting saliva, rise 100- or even 1000-fold
after toothbrushing with F toothpaste.138 This
level drops over the next few hours, with some
of the salivary F being taken up by plaque.
Postbrushing levels of intraoral F are affected by
the amount and vigor of rinsing after brush-
ing53; the best advice for adults is to rinse gently
after brushing.
Because laboratory studies showed that the
uptake of F into demineralized enamel and into
plaque was proportional to the concentration
of F in the toothpaste, a natural next step was
the testing of toothpastes with higher concen-
trations. Toothpastes with 1500 ppm F have
been found slightly more efficacious than
the 1000-ppm F products.36,62,118 A review of
the action of these higher-concentration tooth-
pastes concluded that an MFP toothpaste with
1500 ppm F reduced the caries increment by

another 12% over that achieved by the standard
F toothpastes with 1000-1100 ppm F,134 although
the results of studies with toothpastes contain-
ing mixed F compounds were more equivocal.
Clinical trials have also been conducted with
toothpastes of 2500 ppm F or more with mixed
results. Studies in Scotland, testing several
products, found that caries reductions were pro-
portional to the F concentration in the tooth-
pastes,149 but two North American studies
found no difference between the 2500-ppm
F MFP products and standard-strength F tooth-
pastes.102,135
At the other end of the spectrum, concerns
about the fluorosis risk from the swallowing of
toothpaste by children have led to the testing
of toothpastes with lower than standard levels
of F for use by children. The first clinical trials
compared products with 250 ppm F against
those with 1000 ppm F and yielded conflicting
results.92,113 Findings from later studies of 500-
to 550-ppm F products, however, suggested that
they may be no less efficacious than 1000-ppm
F toothpastes.159,168 Because children can swal-
low between 0.12 and 0.38 mg of toothpaste
per brushing,20 the marketing of lower-F tooth-
pastes is likely to reduce the risk of fluorosis
while substantially retaining caries-preventive
benefits. Toothpastes containing 400 ppm
F have been available in Europe, Australia, and
New Zealand for years, although these 400-
ppm F products have not been tested in clinical
trials. They are not available in the United States
and Canada, despite strong calls to market these
child-strength toothpastes in North America.
Use of F toothpastes has just about been
institutionalized in the United States and in
many other countries. It is hard to find a tooth-
paste that does not contain F, and manufactur-
ers no longer bother to use F content as part
of their advertising. Further research can be
expected to focus on determining the most
favorable formulations of F plus abrasive and
the most appropriate F concentrations. A wel-
come development, alluded to already, would
be the marketing of children’s toothpastes of
500-550 ppm F separately from adult-strength
products, which might be 1500-2500 ppm F.
The principal reason for the absence of adult-
strength F toothpastes is that the swallowing of
F toothpaste by children is a risk factor for fluo-
rosis (see Chapter 22); thus, if children swallow
26 Other Uses of Fluoride in Caries Prevention 357
higher-F toothpaste, then the prevalence and
severity of fluorosis may get worse. On the other
hand, higher-F toothpastes are likely to be more
beneficial in preventing coronal and root caries
in adults than the first-generation products.
Perhaps the market could manage both forms
of toothpaste with appropriate color coding
and warning labels on the high-F products.
Standards for Toothpaste Efficacy
The toothpaste market is a multibillion-dollar
industry in the United States, so competition
between major manufacturers is keen. Compa-
nies incur much research and development
expense to secure the ADA’s seal of approval
for their products; the logo on the package
improves marketing and is a guide for con-
sumers as well. Because of the multitude of for-
mulations of F plus abrasive available, the ADA
developed guidelines for use in judging applica-
tions for its seal of approval for F toothpastes.10
With newer formulations replacing earlier prod-
ucts and advertising claims being made of supe-
riority over rival products, the ADA went further
in 1988, conducting a workshop to determine
what evidence would be adequate to substanti-
ate claims of equivalency or superiority of a par-
ticular formulation (i.e., F ingredient with
compatible abrasives) relative to other formula-
tions.11 The workshop determined that such
claims always had to be backed by rigorous clin-
ical trials in human populations and that such
trials required the use of the rival product as a
positive control. The trials had to be designed to
show a 10% difference in caries increment with
a power of 80% (see Chapter 13). The ADA’s
seal of approval goes to particular formulations
rather than to products. The list of toothpastes
that carry the seal, which can be found on the
ADA website, is now quite long and seems to be
constantly growing.
Global Impact of Fluoride Toothpastes
The impact of F toothpaste use on global caries
experience has been profound. F exposure is
accepted as the main reason for the decline of
dental caries over recent years, and most author-
ities believe that F toothpaste has been the most
important F vehicle on a global scale.27 The
caries reductions of 15%-30% achieved in most
clinical trials may appear modest compared to
those attributed to water fluoridation, but it
358 Prevention of Oral Diseases in Public Health
must be remembered that these were trials of
2-3 years’ duration, whereas water fluoridation
studies usually measured lifetime exposure.
Because, as we know, F works most effectively to
prevent caries when small amounts are in the
oral cavity at all times, there is no reason why
regular lifetime use of F toothpaste should not
give results that are similar to those of lifetime
use of fluoridated water.
MULTIPLE FLUORIDE EXPOSURES
The majority of clinical trials of F products test
only a single agent. In the modern world, how-
ever, exposure to multiple sources of F is the
rule rather than the exception. People who
live in fluoridated areas brush their teeth
with F toothpastes and are periodically given
professional F applications by their dentists.
F mouthrinsing is used in public health pro-
grams, and some cosmetic mouthwashes con-
tain F. Then there are dietary supplements,
whether used appropriately or not, as well as
the poorly quantified F exposures from food
and drink. When these are added together, it
becomes readily apparent that people in most
high-income countries are being exposed to
much more F than they used to be.
This phenomenon of multiple F exposures
can be viewed from several perspectives. In one
way it is beneficial because, with the several dif-
ferent anticaries actions of F (see Chapter 24),
fuller advantage is being taken of F’s potential.
On the other hand, the increasing prevalence of
fluorosis (see Chapter 22) is almost certain to be
a product of these multiple and poorly con-
trolled F exposures. Dentistry’s goal, though not
an easy one to achieve for either an individual
patient or the community, is to maximize the
benefits from F exposure while avoiding an unac-
ceptable level of the undesirable side effects.
Multiple F therapies, whether in fluoridated
or nonfluoridated areas, are clearly beneficial
for patients who are unusually susceptible to
caries. For example, excellent results in prevent-
ing caries were achieved in patients who had
received radiation treatment for oral cancer,
a treatment that can produce dysfunction of the
salivary glands and hence loss of salivary buffer-
ing capacity. The therapy included F gel-tray
applications, daily F mouthrinsing, and routine
use of F toothpaste.49
Caries reductions above those expected from
fluoridated water alone have been found
among children in fluoridated areas who
(1) underwent annual topical applications of
SnF2,76 (2) received F mouthrinses and gel-tray
applications in combination,68 or (3) per-
formed intensive self-application of F using cus-
tom-made trays.56 An 11-year demonstration
project, begun by the National Institute of
Dental Research in 1972, provided F supple-
ments, F mouthrinses, and F toothpastes to chil-
dren in a poor rural area. The intention was to
show that school-based combined F programs
could reduce caries experience in rural areas.78
Cohorts of 1983 participants had MF (decayed,
missing, and filled) scores that were 65% lower
than those in baseline cohorts in 1972. The
demonstration was unfortunately not designed
to permit identification of the individual effects
of the different F regimens, and the absence of
concurrent controls made interpretation of the
caries reductions uncertain.
In the context of cost effectiveness, the data
on the use of F mouthrinses in fluoridated areas
are worth examining in detail: Table 26-3 pres-
ents these data for five North American stud-
ies. A beneficial effect can be seen in each case,
although even in the earlier studies the effects
were limited in terms of absolute caries reduc-
tions. A later study of multiple F exposures
measured the comparative impact of F tablets
and F rinses. 51 After 8 years children who
both ingested the F tablets (after chewing)
and rinsed weekly with neutral 0.2% NaF
solution had a caries increment that was
33% lower than that for children who rinsed
only and 15% lower than that for those
who took the supplements only. However, in
the age of low caries experience the largest
absolute difference between groups was only
1.17 DMFS (decayed, missing, or filled tooth
surfaces) over the 8 years. Cost-effectiveness
issues arise given results such as these: when a
new F program is instituted among children
who already have some F exposure and low
caries experience, is the additional benefit
worth the cost?
The last two lines of Table 26-3 showing data
from the NPDDP provoked the subsequent crit-
icisms of F mouthrinsing mentioned earlier
in this chapter. Table 26-4 gives the results of
studies in which supervised brushing with an
 26 Other Uses of Fluoride in Caries Prevention 359

Table 26-3 Summarized results of studies of fluoride mouthrinses in fluoridated areas

Material Age-Groups Duration % Reduction DMFS Reduction Reference

0.1% SnF2 daily 8-13 yr 20 mo 33.1* 1.00 Radike et al128

43.3† 1.22
0.05% NaF daily 12 yr 30 mo 27.9* 0.72 Driscoll et al52
49.7* 0.94
0.2% NaF weekly 12 yr 30 mo 22.1* 0.57 Driscoll et al52
55.0† 1.04
0.2% NaF weekly 9 yr 24 mo 33.8 0.52 Kawall et al87
0.2% NaF weekly Grades 1-2 48 mo Not given‡ 0.29 Bell et al19
Grade 5 24 mo Not given‡ 0.03
DMFS, Decayed, missing, and filled tooth surfaces.
*First of two examiners.
†Second of two examiners.
‡Could not be determined from the data provided.

Table 26-4 Summarized results of studies of additive effects of fluoride mouthrinsing and supervised brushing
with fluoride toothpastes DMFS Increments
Rinse +
Age-Groups Duration F Rinse* F Toothpaste† Toothpaste‡ Placebo Reference

Approximately 24 mo 4.81 4.44 4.12 5.61 Ashley et al13

13 yr (13.1%)§ (17.9%)§ (22.7%)§
11 yr 30 mo 4.79 5.14 5.30 6.51 Ringelberg et al131
(23.4%)§ (17.8%)§ (15.2%)§
10-13 yr 30 mo None 6.30 5.60 None Triol et al158
(11.1%)¶
11-12 yr 36 mo 4.72 4.60 4.76 6.25 Blinkhorn et al24
(24.5%)§ (26.3%)§ (26.8%)§
DMFS, Decayed, missing, and filled tooth surfaces.
*0.05% NaF daily at school.
†0.76% Sodium monofluorophosphate except for Ringelberg et al79 (0.4% stannous fluoride, unsupervised).
‡All conducted supervised rinse immediately after brushing.
§Percentage reduction compared to placebo control.
¶Percentage reduction compared to sodium monofluorophosphate toothpaste alone.

F toothpaste was combined with supervised
daily F mouthrinsing at school, and the results
were compared with those for each procedure
alone. The results for the combined procedures
are, at best, only slightly superior to the use of
either alone. Scandinavian studies, not included
in Table 26-4 because they tested weekly or fort-
nightly rinsing and unsupervised home use of
an F toothpaste, also reported little added bene-
fit from the rinsing programs at school.15
Because caries experience in North American
children has generally reached lower levels than
those at which the results in Tables 26-3 and 26-4
were produced, it is hard to argue for the cost
effectiveness of F mouthrinsing in fluoridated
areas, especially where frequent use of F tooth-
paste is common. This conclusion was confirmed
at the 1989 workshop on cost effectiveness of pre-
ventive programs.130
Cost effectiveness is a less important issue
for the private patient than for public health
programs, but selection of a preventive regimen
for an individual patient should still take
into account the likely added benefit of
multiple exposures. To illustrate, professional
F applications are of dubious additional value to
the individual patient in a fluoridated area who
brushes daily with F toothpaste and who has lit-
tle caries problem. However, even in a fluori-
dated area, more caries-susceptible patients may
360 Prevention of Oral Diseases in Public Health
get reasonable additional benefit from profes-
sional F gel applications or prescribed daily use
of F mouthrinses. In these decisions, the clinical
judgment should always be guided by experi-
mental data and can be enhanced by attention
to the CDC recommendations on F use.162 As we
have said already, however, broad exposure to
multiple sources of F is the norm in North
America today. When introducing a new F pro-
gram in a community, therefore, a public health
administrator must assess whether the program
will produce benefits beyond those already
being provided by other F exposures. The evi-
dence just cited shows that additional benefits
will probably accrue, but the bigger public
health question is whether the extra benefits will
be worth the cost of the program.
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 27 Fissure Sealants
HISTORICAL DEVELOPMENT
RATIONALE FOR SEALANTS
SEALANT PRODUCTS AND PROCEDURES
SEALANT CLINICAL TRIAL DESIGN
SEALANT EFFICACY
All ADA-Approved Sealant Types Have Similar
Efficacy
Sealants Can Be Safely Placed over Incipient
Caries
A fissure sealant is a plastic, professionally
applied material used to occlude the pits
and fissures of teeth. The purpose is to provide
a physical barrier to the impaction of sub-
strate for cariogenic bacteria in those crevices
and hence to prevent caries from developing.
Sealants also can halt the carious process after it
has begun and can be used as a form of treat-
ment for early lesions. All sealants are applied
to the tooth in liquid form and polymerize (or
“cure”) in place a short time later.
The correct name for this group of materials
is pit-and-fissure sealants, but they are more com-
monly referred to as fissure sealants, or just
sealants (the term we will use). This chapter dis-
cusses the use of sealants in caries prevention,
examines the issue of their cost effectiveness,
and makes recommendations for their use.
HISTORICAL DEVELOPMENT
The idea of physically occluding pits and fis-
sures is hardly new, for as long ago as 1923
Hyatt suggested a technique he called “prophy-
lactic odontotomy.”52 Developed in an age of
severe and seemingly universal caries, Hyatt’s
technique involved minimal operative pre-
paration of sound fissures and restoration
with amalgam. The idea was not fully accepted
even before the days of modern preventive
366
Sealants Are of Uncertain Value on Primary
Teeth
Sealants Are an Important Part of Public
Health Programs
SEALANTS IN PUBLIC PROGRAMS
COST EFFECTIVENESS OF SEALANTS
PUBLIC AND PROFESSIONAL ATTITUDES
TOWARD SEALANTS
dentistry,58 but it led to widespread use of the
“preventive restoration,” meaning a full Black’s
cavity restoration with “extension for preven-
tion” in sound fissures, placed on the grounds
that without intervention such areas would
soon decay anyway. For many years, this type of
restoration was considered good preventive
practice, and perhaps it was when there were
few other preventive options. Although we have
no way of knowing just how much caries this
method “prevented,” the extensive use of the
preventive restoration served to artificially
inflate DMF (decayed, missing, and filled)
scores (see Chapter 15).55
In the prefluoride era, various chemicals
were painted onto the tooth surface in an effort
to prevent caries, but none proved success-
ful.11,57 Even after fluoride entered dental prac-
tice, interest in a specific preventive agent
for pit-and-fissure caries persisted, but it proved
difficult to find a material that adhered success-
fully to enamel in the oral environment. The
breakthrough came in 1955 with Buonocore’s
development of the acid-etch technique.21 By
the mid-1960s cyanoacrylates had been used
as sealant materials with some success,30
but their production was not continued.91
In the late 1960s the “bis-GMA” formulation
(a sealant that is the reaction product of bisphe-
nol A and glycidyl methacrylate with a methyl

methacrylate monomer) was developed and
proved successful in a feasibility trial.22 The bis-
GMA formulation became the basis of a num-
ber of other products that soon came onto the
market. The American Dental Association
(ADA) issued provisional acceptance of the
first bis-GMA material, Nuva-Seal, in 19724
and full acceptance in 1976.5 The number and
types of accepted materials have grown steadily
since then and will likely continue to grow in
the future. Currently, the most widely used
sealant materials are either bis-GMA resin or
urethane based.109 There is also considerable
interest in the potential use of glass ionomer–
based materials and fluoride-containing var-
nishes as sealant materials, but the research
literature to date shows their retention to be
inferior to that of the conventional sealant
materials.9,16,17,56,69-71,96,97,105,116
RATIONALE FOR SEALANTS
It has been recognized for years that fissured
occlusal surfaces are the most vulnerable to
caries. With the continuing caries decline
among children, caries is more and more a dis-
ease of the fissured surfaces as the rate of inter-
proximal caries development continues to
decline faster than the overall rate of caries
experience.13,99 Occlusal surfaces are also those
least protected by fluorides,12 so the case for
sealant application as a complementary proce-
dure to fluoride use is even stronger. As of the
early 1990s, at least 83% of all decayed or filled
surfaces in the permanent teeth of 5- to 17-year-
olds were in pit-and-fissure surfaces.19 In fact,
the appropriate delivery of fluorides and
sealants together, in theory at least, presents the
prospect of controlling caries to low levels pre-
viously unimaginable.
SEALANT PRODUCTS
AND PROCEDURES
The original bis-GMA materials, now referred to
as first-generation sealants, polymerized under
ultraviolet (UV) light, a procedure that required
a bulky UV light source in the oral cavity.
Second-generation sealants are chemically
polymerized; that is, when they are mixed, the
operator has a fixed time to apply the sealant
before it hardens. A number of such sealants are
27 Fissure Sealants 367
currently available. Third-generation sealants
are those cured by visible light, which gives the
operator the advantage of curing the sealant
only when satisfied that it is all correctly
in place. That advantage also applied to first-
generation UV-cured sealants, but the visible
light sources are far more compact and less
expensive than the original UV light sources.
Some second- and third-generation sealants are
colored or opaque to make them more visible at
clinical examination.
It should also be noted that in 1996 a
research report from Spain concluded that,
shortly after placement of sealants, bisphenol A
and bisphenol A dimethacrylate monomers
could be detected in saliva and that these
monomers showed estrogen-like activity when
tested in in vitro cultures of human breast cell
tumors.68 This effect is of concern, because it
theoretically could result in increased tumor
cell growth. To date there is no evidence that the
transient amounts of these chemicals in saliva
represent an important exposure in humans. In
addition, none of the sealants that currently
carries the ADA seal of acceptance produces
detectable levels of bisphenol A.1 However, the
Spanish finding does point out that any mate-
rial used in dentistry must be thoroughly evalu-
ated for potential risk and that, regardless of
how safe it appears to be, practitioners must
take care to use any procedure or material only
when the patient is likely to benefit from it.
The ADA provides continual updates on these
and related matters on its website (http://www.
ada.org/prof/resources/positions/statements/in
dex.asp).
Sealant application is a simple though metic-
ulous procedure that requires attention to all
details of technique, especially moisture con-
trol. Even slight moisture contamination during
sealant application and curing will result in fail-
ure. When applying a sealant, the operator
begins by washing and drying the tooth surface,
then etching with acid to demineralize the
surface layers of enamel in and around the
fissures. The etchant is supplied as either a
liquid or a gel; 35%-37% orthophosphoric acid
is the most commonly used agent.109 Acid etch-
ing dissolves out some of the inorganic fraction
of the enamel, which subsequently allows
“tags” of sealant to penetrate and thus enhances
retention. Some of these tags can extend up to
368 Prevention of Oral Diseases in Public Health
100 μm into enamel, although tags of 15-20 μm
are more common.92 After etching, the tooth
surface is again washed and dried thoroughly,
and the liquid sealant is applied and worked
into the fissures and pits. The sealant is then
polymerized (by visible light or by self-curing)
and trimmed if necessary. Detailed descriptions
of the application process are available.109
By the early twenty-first century, the applica-
tion of sealants as a purely caries-preventive
procedure was merging into the popularity of
conservative restoration procedures, many of
which also used the acid-etch technique. The
trend was stimulated by the caries decline,
which meant that practitioners increasingly
had to manage small, slowly developing lesions
rather than large cavities, and by the rapid devel-
opments in composite materials. Dentistry
began moving away from placement of amal-
gams in traditionally prepared Black’s cavities
with extension for prevention and toward mini-
mum-preparation restorations, which were far
less invasive, lasted longer, and were more
esthetic.35 The preventive resin and sealed com-
posite restoration,49,63,110 sealed glass ionomer
restoration,46 “tunnel” restoration for small
proximal restorations,28 and even sealed amal-
gams63,64 are changing the face of restorative
dentistry. The distinction between a purely pre-
ventive sealant placed on a sound tooth, sealant
placed on an incipient lesion, and a minimum-
preparation sealed restoration is becoming
increasingly blurred. The challenge is to under-
stand the indications for each and to use each
appropriately.
SEALANT CLINICAL TRIAL DESIGN
The initial clinical trials for testing the efficacy
of sealants necessarily differed from the
classical model (see Chapter 13) in several
respects:
●
The study design was usually “half-
mouth,” in which the analytic unit is a con-
tralateral pair of teeth, usually first or
second molars. Because test and control
teeth are in the same mouth, the required
number of study subjects (see Chapter 13)
could be reduced.
●
There was no placebo sealant; the control
tooth of each pair in these earlier trials was
simply left untreated (a passive control).
●
Examiners could not be blinded in a trial
with a passive control, for they could see
the sealant on the test tooth.
Because of the overwhelming weight of the
evidence for the efficacy of sealants, recent trials
testing new products now most commonly
apply an accepted sealant as a positive control
on the control tooth or individual dentition.
Because positive controls are used in compara-
tive studies, the examiners should be blind as to
which sealant is the test product and which is
the positive control. Because differences in effi-
cacy between the test product and the control
are expected to be small, the numbers of sub-
jects needed is fairly high.
SEALANT EFFICACY
A large number of well-conducted sealant stud-
ies have been carried out, which allows conclu-
sions on their efficacy to be stated with some
confidence. The panel at the National Institutes
of Health Consensus Conference on dental
sealants in 1983, one of the relatively few such
conferences held on dental procedures, con-
cluded that sealants were highly efficacious.67
The panel also noted, however, that practitioners
were slow to adopt their use and that insurance
carriers were also hesitant about adding sealant
application to their list of benefits. The Medicaid
programs in all 50 states now cover sealant
application, and although precise numbers are
unavailable, the number of privately insured
groups with sealant coverage continues to grow.
The first clinical sealant studies in the 1960s
yielded spectacular results, with caries reduc-
tions of 99% reported.22 These initial studies,
however, carefully selected both the patients
and the teeth to be sealed. By the end of the
1970s, there was clear evidence from numerous
clinical trials in different populations that
sealants were highly efficacious when applied
correctly.76 Studies since then using second-
and third-generation sealants have almost all
yielded results highly favoring their use; reviews
of what is now an extensive literature have all
reached highly favorable conclusions regarding
their efficacy.77,78,100,113 Well-controlled clinical
trials have shown good results after 5 years,48
7 years,65 and 10 years78; and 10-year and
15-year retrospective reports also showed
encouraging results.94,95 The favorable evidence

has led the ADA to strongly support the appro-
priate use of sealants in general practice.2,3
Evidence for the efficacy of sealant applica-
tion in private practice, although scanty, also
appears favorable. In an observational study in
Canada, sealed first permanent molars had a
75% lower incidence of new restorations than
originally sound but unsealed molars.53 The
authors acknowledged that use of sealants was
more common in caries-free children and in
children whose parents had higher levels of
education, which could account for some of the
lower caries increment, but the differences in
caries experience were so large that sealants had
to have played a substantial role. It is neverthe-
less important to be cautious in interpreting
outcomes from observational studies in which
patients are not randomly assigned to receive or
not to receive sealants. As has been pointed out
in a study of the use of sealants in a Medicaid
program, the children who actually received
sealants tended to be at lower risk; that is, they
were more likely to have been caries free ini-
tially and were more likely to have been classi-
fied by the study examiners as not needing
sealants.80 The authors pointed out that this
pattern of nonrandom use of sealants in the
least caries-prone children could lead to overes-
timates of sealant effectiveness. Nevertheless,
there is ample reason to think that, with appro-
priate patient selection, sealant application is
highly effective in private practice.
Findings from the earlier clinical studies of
sealants that have been supported by later
research include the following:
●
Sealant is generally retained better on
mandibular than on maxillary molars. This
is attributed to better accessibility and
more favorable tooth morphology.
●
Sealants are better retained when placed in
older children. This is thought to be due to
the ability to achieve better isolation in
more completely erupted teeth and the
ability of the older child to cooperate in
maintaining a dry field.
●
Retention seems better on bicuspids than
on molars. This too is likely to come from
better accessibility, plus the fact that in
studies in which children have had bi-
cuspids sealed they were obviously older
than children who had only their first
molars available for sealing.
27 Fissure Sealants 369
●
Retention of sealant is synonymous with
freedom from caries. An early concern was
how the caries status of a tooth could be
judged beneath intact sealant, but subse-
quent clinical research has shown that
caries does not progress beneath intact
sealant.
●
Loss of sealant is greatest in the first
6 months after application. The sealant is
probably lost very early in that period,
however, because the data suggest that the
rapidly lost sealants are those that never
properly adhered in the first place. The
most likely reason for this kind of failure is
moisture contamination. A properly placed
sealant will gradually wear down after a
period of years, but protection from caries
seems to remain, perhaps because of the
sealant tags. The quickly lost sealant almost
certainly has no tags, so the tooth con-
cerned becomes vulnerable again.
These results demonstrated unequivocally
the considerable efficacy of sealants; they also
gave hints of the more recent realization that
sealants are more difficult to successfully apply
and maintain on the very teeth that are most
vulnerable, that is, the early-erupting molars in
caries-prone children. On the other hand,
sealants seem to be retained best on teeth that
are least caries prone (e.g., bicuspids) and in
children with low caries risk.18 This realization
is part of what has lead to efforts to target
sealant use to the most susceptible groups, indi-
viduals, and teeth, an issue discussed later in
this chapter.
Later studies of sealant efficacy have led to
four additional conclusions that have an impor-
tant bearing on the way sealants are used in
clinical practice. These conclusions are dis-
cussed in the following sections.
All ADA-Approved Sealant Types Have
Similar Efficacy
With the evolution of sealant systems and the
large number of brands now available, it is
logical for dentists to ask which type is best.
The response from clinical studies is that
all accepted sealants are effective when
applied properly. Results of numerous trials
have demonstrated that the retention of the
light-cured sealants is equivalent to that of the
chemically polymerized products.50,81,102,117
370 Prevention of Oral Diseases in Public Health
No UV-cured sealants have been among the
list of ADA-approved sealants for a number of
years, because they have been superseded by the
chemically polymerized and visible light–cured
sealants. The dental practitioner’s choice thus
comes down to personal taste: an autopolymer-
ized sealant hardens a specified time after
preparation, just like many other products used
in dentistry. The visible light–cured resins
require the handling of an extra piece of equip-
ment, the light source, but setting time is con-
trolled by the operator.
Sealants Can Be Safely Placed
over Incipient Caries
A conclusion of the National Institutes of
Health consensus panel in 1983 was that
evidence supported the use of sealants to
arrest the progress of incipient lesions.67
Nothing has occurred since then to alter that
conclusion.
Modern sealants were developed as a pri-
mary preventive procedure—that is, to be
placed on sound surfaces—but shades of
Hyatt’s philosophy soon emerged. Given that
sealants occluded the fissures, it was logical to
question whether caries could progress beneath
a sealant. The answer, after a number of studies,
is now clear. When a sealant is placed over an
incipient carious lesion, meaning a stained fis-
sure in which softness at the base can be
detected but in which cavitation has not yet
occurred, caries does not progress provided
the sealant remains intact. Sealant is retained
on the carious teeth just as well as on sound
teeth,42 and neither lesion depth nor microbio-
logic counts progresses under intact sealant.41,66
Reviews of these and other studies have con-
cluded that the evidence is strong that caries-
active lesions become caries inactive beneath
intact sealant.38,103 As restorative philosophy
continues to evolve toward increasingly conser-
vative cavity preparations, more recent reports
confirm that even carious dentin, when isolated
under a minimal restoration and sealant, does
not progress.63 These results provide further
assurance that the clinician need not fear the
placement of sealant over incipient caries.
Indeed, as discussed later in this chapter, con-
sensus is developing that the placement of
sealants over incipient lesions is one of their
most effective uses.
Sealants Are of Uncertain Value
on Primary Teeth
Some early research showed poorer retention of
sealant on primary tooth enamel, although
results were better in some later studies.75,93
The different enamel structure of primary teeth
was thought to be a possible reason, although
moisture contamination may also have been
greater with younger children. Subsequent lab-
oratory studies have shown that a short etch
time is effective for primary enamel,106 and
sealant retention on primary molars in a large
Head Start program in Tennessee was equiva-
lent to that on permanent molars.43 What is not
clear, however, is whether the usual caries pat-
tern in primary molars is compatible with opti-
mal sealant effectiveness, despite retentive
success. In many children, the occlusal surfaces
of primary molars are not highly fissured and
thus are not especially caries prone. Further,
when caries is a problem in primary molars, the
first lesion is often interproximal. Sealants are
not effective in these circumstances.
Sealants Are an Important Part of Public
Health Programs
With the decline of dental caries among chil-
dren, especially interproximal caries, sealant
programs are becoming more appropriate
choices in public caries prevention programs for
children. Although many dental public health
initiatives are directed toward encouraging the
use of sealants in private practice, there is also
considerable activity in the development of
projects to actually place sealants in public pro-
grams. In 2002 29 states reported having
school-based or school-linked sealant pro-
grams, serving 193,000 children.108 These
programs operate either in schools, usually with
portable equipment, or in community clinics.
How effective these programs can be both in
increasing sealant prevalence and in reducing
racial disparities in sealant use is demonstrated
by the data in Fig. 27-1. In the Ohio sealant pro-
grams, the overall prevalence of sealants in
third-grade students was approximately twice as
high in schools with a sealant program as in
those without such a program, and the absolute
and relative racial disparities also dimin-
ished.107 The philosophy behind these public
sealant programs is almost always to bring this

70
White
60 African-American
50
Percent with sealants
40
30
20
10
0
Sealant program No sealant program
Fig. 27-1 Dental sealant prevalence in third-grade children
in Ohio, in schools with and without a dental sealant program,
1998-99.107
preventive procedure to children who otherwise
would be unlikely to receive comprehensive
dental care. School-based and school-linked
programs are targeted to schools with a high
proportion of children from low-income fami-
lies or schools with a high number of children
with untreated dental needs, or to areas in
which there is a shortage of dentists.10
SEALANTS IN PUBLIC PROGRAMS
Research has shown that trained auxiliaries
can apply sealant just as successfully as can den-
tists.25,61 This is an important finding in public
health, for the cost effectiveness of sealant
programs virtually depends on deployment of
auxiliaries.23 It is unfortunate that regulations
in some states do not permit auxiliaries to apply
sealant, a provision that is hard to defend
as being in the public interest. The on-site pres-
ence of a dentist will obviously add to the
cost of a public program without necessarily
improving its outcome. Several public health
sealant programs have managed to deal with
these problems and have subsequently flour-
ished. One is in New Mexico, which required
revision of its dental practice act to permit auxil-
iaries to apply sealant in the state-administered
program.87 The New Mexico program, which
uses mobile teams with portable equipment,
27 Fissure Sealants 371
found 67% retention of one-time sealant appli-
cations after 6 years. In sixth-graders who had
received sealants on their first molars in grades
1, 2, or 3, only 5.6% of those surfaces subse-
quently become carious, compared with 26.9%
of the same surfaces in children who were not in
the sealant program.24 Even allowing for some
self-selection bias, those figures are impressive.
In the Canadian province of Saskatchewan,
79% of sealants applied by dental therapists
were retained 3 years later, and sealed teeth
developed 46% less caries than their unsealed
counterparts after 4 years.54 In Canada’s Prince
Edward Island program, there is annual reseal-
ing when needed. In that province, 85% of
sealants were successful after 8-10 years,83 simi-
lar to results reported for a 10-year study in
Sweden.115
In addition to providing geographic targeting
(see Chapter 4) of sealant programs to schools in
more deprived communities, most public
sealant programs also treat only children at spe-
cific stages of dental development (i.e., soon after
eruption of the first and second molars). In the
United States, where children begin school at
age 6, grades 1-2 are the best times for sealing
first molars, and grades 6-7 for sealing second
molars.14,59 Sealing of bicuspids and primary
teeth is not usually a part of public programs
because far fewer bicuspids decay than do
molars,6,33 and a primary molar that is sound in
grade 1 will probably stay that way. A good body
of experience in the operation of programs with
sealant teams has now accumulated,24,53 and
excellent guides to the development and opera-
tion of public sealant programs are available.26,72
We referred earlier in this chapter to the
prospect of using sealants and fluoride together
to reduce caries-associated problems to lower lev-
els than could even have been imagined only a
few decades ago. Sealant placement is an obvious
adjunct to water fluoridation; a comprehensive
1989 review found that sealants were more effec-
tive in fluoridated areas than in nonfluoridated
areas, although the difference was slight.113
Sealants also have been tested in combination
with fluoride mouthrinsing. In a New York study,
after 2 years the 84 children in grades 2-3 with
sealants had an increment of only 0.03 DMFS
(decayed, missing, and filled surfaces), compared
with an increment of 0.47 DMFS in the control
group. In the 84 children in the sealant-rinse
372 Prevention of Oral Diseases in Public Health
group, there were only 3 new decayed or filled
surfaces over the 2 years, 2 of them occlusal,
whereas in the 51 controls, there were 24 new
decayed or filled surfaces, 15 of them occlusal.79
In another study that used a sequential cross-
sectional comparison group, a 23% decline in
occlusal caries over a 4-year period in 14- to 17-
year-olds was attributed to the addition of sealant
placement to an ongoing school-based fluoride
program.85 These data suggest that nearly
complete prevention of caries at levels that
require invasive restorations is indeed theoreti-
cally possible, but its achievement might be
costly. As we saw with topical fluoride applica-
tion in Chapter 26, there comes a point at which
the underlying risk of caries in some individuals
is so low that additional fluoride exposure is not
warranted. The same is likely to be true for
sealant placement. In those individuals (and
teeth, in the case of sealants) in whom the risk of
occlusal caries is very low, the cost of placing and
maintaining sealants may outweigh the potential
benefit that sealants can be expected to provide.
This is the biggest question a public health
administrator has to deal with when considering
sealant programs: can we afford it, and is the ben-
efit from sealants worth the cost?
COST EFFECTIVENESS OF SEALANTS
Questions arose about the cost effectiveness of
sealants in public programs almost from their
first use. A public health community that con-
sidered water fluoridation to be the gold stan-
dard in terms of the cost effectiveness of public
programs naturally looked askance at this one-
on-one procedure, and an early economic
assessment was not encouraging.36 However, in
this review dentists, rather than auxiliaries,
applied the sealant, and retention of the first-
generation sealant was not high.
Cost effectiveness is defined as use of the least
expensive way, from among competing alterna-
tives, of meeting a defined objective.112 It differs
from cost benefit, which is the ratio of an activ-
ity’s cost to the monetary benefit it produces,
although it is conceptually similar to efficiency,
which is the return on effort expended.111 The
term a cost-effective program is virtually synony-
mous with an efficient program.
The cost-effectiveness issue arises in public
dental programs when a dental director whose
objective is to reduce caries experience in a child
population by a specified amount over a speci-
fied time considers the use of water fluorida-
tion, sealant placement, application of fluoride
varnish, use of fluoride mouthrinses, or dental
health education to meet that objective. The
director weighs the costs of each program
against the anticipated benefit. (In a fluoridated
community in which people routinely use fluo-
ride toothpastes, have high utilization of dental
services, and have very low caries levels, intro-
ducing no new program might also be a rational
alternative.) Thinking in terms of cost effective-
ness has moved dentistry away from an attitude
of “the more prevention the better” to careful
selection of which programs are likely to be the
most efficient. Cost effectiveness is also at the
root of discussions on targeting preventive pro-
grams to the most susceptible groups and indi-
viduals rather than applying them across the
board (see Chapters 4 and 20).
Are sealants expensive? That depends on what
they are compared with. For example, compared
to fluoridated water and other types of self-
applied fluorides, sealants are a relatively expen-
sive alternative requiring application by a
professional. In terms of fees charged by dentists
in private practice, the average fee for a sealant
application has remained at approximately 50%
of the fee for a one-surface amalgam restoration.
The ADA’s 2001 survey of fees charged by general
practitioners in private practice found that the
mean fee for sealant application was $31.89 per
tooth, whereas the mean fee for placement of a
one-surface amalgam in a posterior permanent
tooth was $73.21 and for a one-surface composite
resin restoration on a posterior tooth was $98.17.7
In public programs, it has been shown that sealant
application can be even less expensive. The aver-
age cost of providing a sealant in public programs
in the mid-1990s was $8.17 per tooth, well under
the average of $24.42 charged in private offices
as of 1995.10 The ability to provide sealants at
lower cost in public programs is attributable in
part to the economies that are possible through
treating large numbers of children in a “captive”
setting in schools and through the extensive use of
auxiliary personnel to place the sealants.
The other side of expense is effectiveness. The
evidence cited earlier shows that sealants are
highly effective; their widespread use can
have an immediate and substantial impact on

the caries experience of a group that would
otherwise experience occlusal caries. Although
there are few specific studies on the relative
cost effectiveness of sealants and other pre-
ventive procedures, a 1989 workshop gave
sealants a favorable cost-effectiveness review,
rating them slightly higher in nonfluoridated
areas because of the higher probability of caries
attack.73 This means that sealant application is
not only a logical public health program to
choose in light of caries distribution in the
early twenty-first century, but it may well be
one of the more efficient ones as well. However,
it must be stated that the cost-effectiveness
issue is far from settled and is really wide
open for additional research. To illustrate,
readers may have noted the vexing conundrum
that, whereas sealants may be more effective
in fluoridated areas,113 the 1989 workshop
concluded that they are likely to be more
cost effective in nonfluoridated areas.73 This
is the case because, although in a fluoridated
area a higher percentage of carious lesions will
be on occlusal surfaces and thus prevent-
able with sealants, in a nonfluoridated area,
there will actually be a higher total number
of occlusal lesions that could potentially be
prevented.
In the context of the targeting issue, it follows
that sealants would be more cost effective if
they could be applied to the teeth with the
greatest probability of decaying, so that they
would not be “wasted” on teeth that would not
decay anyway. Although prediction methods are
not yet precise enough to accomplish this for
sound teeth, an obvious approach with sealants
is to take advantage of their demonstrated effi-
cacy when applied to early lesions. The cost
advantage of this approach was demonstrated
more than 20 years ago62: sealant application
showed a benefit-cost ratio of only 0.3:1 in
caries-inactive subjects but of 1.02:1 in caries-
active subjects. In another study, the most favor-
able cost-effectiveness ratios were found when
sealant placement was limited to children who
already had restorations in one or more first
permanent molars.114 In yet another school-
based study, although sealants were effective
overall, their effect was especially striking on
surfaces that were initially diagnosed as having
incipient lesions.45 Table 27-1 summarizes
some of the data from that report. These data
27 Fissure Sealants 373
indicate that, over a 5-year period, in surfaces
that were initially diagnosed as sound, 8.1% of
those that were sealed and 12.5% of those that
were not sealed became carious. On the other
hand, of those teeth initially diagnosed as hav-
ing incipient caries (i.e., they had dark staining
or a chalky appearance, or caused a slight “stick”
of the explorer but had no visible enamel sur-
face defect), 10.8% of those that were sealed
became carious, compared with 51.8% of those
that were not sealed. Similarly, interim results
from a clinical trial44 in which teeth determined
not to require restorations were randomly
assigned to receive or not receive sealants
showed the same type of gradient according to
baseline diagnosis. Fig. 27-2 shows that, after an
average of 26 months of enrollment in the
study, 3% of the sealed teeth that were initially
diagnosed as sound required restorations,
whereas 6% of sound teeth not sealed required
restorations. In the case of teeth initially rated
as having a questionable area, 20% of the
sealed teeth required restoration, whereas 41%
of such teeth that were unsealed required
restorations. Of those diagnosed as having
incipient, noncavitated lesions, 39% and 60%
of sealed and unsealed teeth, respectively,
required restoration. Finally, in a retrospective
study of an insured population, which was nec-
essarily an observational study, it was found
that, in the 5 years after eruption, both first and
second molars that were sealed were restored
slightly over one-half as often as unsealed teeth
(Fig. 27-3).31
Taken together, the data from these various
studies show two things very clearly: first, that ini-
tial diagnosis makes a very large difference, at
least in the short term, with regard to the value of
Table 27-1 Percentage of surfaces (absolute
numbers in parentheses) becoming carious after 5
years in sealed and unsealed first permanent molars,
by initial diagnosis45
Initial Diagnosis
Sound Incipient
Sealed 8.1% 10.8%
(24/297) (41/380)
Nonsealed 12.5% 51.8%
(8/64) (29/56)
374 Prevention of Oral Diseases in Public Health

70

Sealant
60
No sealant

Percent restored 50

40

30

20

10

0
Sound Questionable Incipient

Fig. 27-2 Requirement for restoration of permanent molars in children by initial diagnosis and sealant placement,
after 26 months of enrollment in the study.44

25
comes of three sealant strategies: sealing all, none,
Sealant
or a targeted subset of permanent molars. In this
No sealant
20 analysis, if caries increments were high and
sealant costs were low, a strategy of sealing all
would be most cost effective. On the other hand,
Percent restored

15 if caries levels were low and sealant costs were

10
5 likely to be much more efficient than a blanket
0 tinues to decline, the need for selective use of
First molars
Fig. 27-3 Restoration prevalence after 5 years in sealed
and unsealed first and second permanent molars in an
insured population.31
sealants; and, second, that in the “real world”
sealants are not successful 100% of the time.
Although the placement of a sealant reduced the
risk that a subsequent restoration would be
required in all cases, some risk of needing a future
restoration still existed, especially when the initial
diagnosis was of a questionable or incipient
lesion. These observations are also in agreement
with the findings of a simulation and sensitivity
analysis40 that compared the likely costs and out-
high, a targeted strategy would be preferable.
These results suggest strongly that applying
sealants only to those teeth with early lesions or
to the teeth of children with a history of caries is
sealing of all potentially at-risk teeth. It is worth
remembering, too, that if caries incidence con-
Second molars sealant in this way becomes even greater if the
material is to be used efficiently. Use of sealant
only on incipient lesions is, in effect, using it as
an early restoration rather than as primary pre-
vention, an approach that may require a differ-
ent mindset in prevention-oriented dentists. It
also further blurs the distinction between the
use of sealants as primary preventive agents
and their various uses in minimal-preparation
restorations, as discussed earlier.
There are cost-effectiveness issues in private
practice too, although they differ from those in
public programs.2,6 After all, the value of pre-
ventive care eventually depends on what the
individual thinks it is worth. A dentist is proba-

bly justified in sealing a number of teeth in a
patient who wants prevention at any price, even
if the dentist believes, for example, that the
bicuspids being sealed are unlikely to decay.
The more pertinent issue facing a practitioner is
whether to seal or restore a deeply fissured
molar with a suspicious fissure. Is it valid to
compare these two options on a cost-effective-
ness basis? Some commentators have said no,
because one is a preventive procedure and the
other is restorative.47,77,98 Perhaps, but if a
sealant is viewed as a noninvasive restoration,
then it becomes a valid comparison. One study
directly compared the costs of sealing a caries-
free molar with the costs of restoring the carious
contralateral molar with amalgam. When all
maintenance care was taken into consideration,
including necessary replacements of both
sealant and amalgam, the average cumulative
time to place and maintain a sealant over
7 years was 10 minutes 45 seconds; for an amal-
gam it was 14 minutes 26 seconds.101 Another
small-scale follow-up of 12 pairs of children
concluded that treatment costs in children who
did not receive sealant was 1.64 times greater
than the costs in a group who had sealant main-
tained over the period.94 Although these data
are not conclusive, collectively they suggest that
appropriate use of sealants on early lesions is
efficacious, conserves tooth structure, and is
likely to be cost effective. As caries experience
continues to decline, the use of sealants is likely
to be focused even more on the early lesion
rather than the totally sound tooth.
PUBLIC AND PROFESSIONAL
ATTITUDES TOWARD SEALANTS
The slow adoption of sealants by practitioners,
despite the excellent results in many studies, has
been puzzling. Even the main pediatric dental
organizations in the United States did not
adopt policies to encourage the use of sealants
until 1983.8 In a series of conferences and sym-
posia in the early 1980s that addressed the slow
adoption of sealants, the reasons given for
dentists’ hesitancy included skepticism about
efficacy, fear of “sealing in decay,” and failure of
many third-party carriers to cover sealant
application. Virtually identical reasons were
still given by dentists who were not using
sealants as recently as 1992.90 Many dentists
27 Fissure Sealants 375
also expressed a sublime faith in the longevity
of amalgams, a faith that research shows is seri-
ously misplaced.6
Even though the trend to more widespread
use of sealants has developed slowly, it is
consistent. Some growth in the numbers of den-
tists using sealants was evident through the
1980s,29,51,82 and by the early 1990s several
states reported that more than 90% of general
dentists were using sealants.15,39,90 Growing
acceptance of the use of sealants over incipient
lesions was also evident. In a 1985 survey in
Washington state, only 18% of dentists who
used sealants reported doing so over incipient
lesions,27 but in 1992 more than 77% of Ohio
dentists reported a willingness to seal over
incipient caries, at least under some circum-
stances.90 This trend toward more widespread
use of sealants is likely to continue, because the
dentists most likely to use sealants are the
younger, more recent dental school graduates,90
and the acceptance of sealants by patients
appears to be heavily influenced by the recom-
mendations of their dentists.60,84,90
Data on the prevalence of sealants in national
surveys also show that their use is increasing.
Data from the 1986-87 national survey of
U.S. schoolchildren ages 5-17 years indicated
that 7.6% had one or more dental sealants
on permanent teeth.20 By 1991, however, the
results from the first part of the third National
Health and Nutrition Examination Survey
(NHANES III) showed that this proportion
had risen to 18.5%.86 Although this increase is
encouraging and is likely to continue, a note of
caution is in order because this higher level of
sealant application will be most helpful if the
sealants are being placed in children who are
most likely to develop carious lesions.89 For
maximum benefit, it is important that dentists
in private practice, as well as those in charge of
public programs, target their sealant applica-
tions to the patients most likely to profit from
them.
The evidence is also consistent regarding the
characteristics of patients who receive sealants.
Higher levels of parental education and income,
and enrollment in a dental insurance program
repeatedly have been shown to be associated
with sealant use.60,84,104 These characteristics
are associated with greater use of virtually all
forms of dental care.
376 Prevention of Oral Diseases in Public Health
Lack of dental insurance coverage has been
cited as a major factor in the slow acceptance of
sealants,37,67,90 although this situation, too,
appears to be improving. By 1994 all 50 states
had included sealant placement as a benefit in
their Medicaid programs,88 and although exact
numbers are unavailable, it is evident that an
increasing proportion of private insurers are
including sealant placement as a benefit.
However, the economic picture for insurers is
not clear, because adding sealant placement to a
benefit package usually requires an increase in
premiums, especially because caries experience,
and thus the need for restorations, continues to
fall.32,34
Although it is evident that dentists and
patients are becoming increasingly comfortable
with the use of sealants, it is also true that the
view as to their most appropriate use continues
to evolve. In the earliest days, sealants were
thought of almost exclusively as a material to be
used on sound pit-and-fissure surfaces to prevent
the development of a carious lesion. As the tech-
nology has developed and the overall caries pat-
tern has changed, there has been an evolution in
thinking. It is now widely accepted that not all
children nor all teeth need sealants. Caries-free
children, in the absence of other indications of
risk, are not good candidates for sealant place-
ment. A key criterion is that the fissured surface
must be at significant risk for disease. This also
has led to the view that sealant placement is
appropriate for older children and adults in
selected cases.2,74,89 In this regard, sealants are
increasingly seen as part of a trend toward much
more conservative restorations.63 Timely place-
ment of sealant on a tooth with an incipient
lesion, with a conservative restoration if neces-
sary, is increasingly viewed as the most appropri-
ate care, regardless of the age of the patient.
As must any other tool in the dental arma-
mentarium, sealants must be used appropri-
ately, in a way that is (1) compatible with the
properties of the material, (2) consistent with
the nature of the condition that they are meant
to prevent or treat, and (3) acceptable in terms
of cost to the provider and patient. Sealants and
the associated composite products are among
the most exciting technologic developments
in dentistry. The technology and the standards
for sealant use will undoubtedly continue to
progress. At the same time, optimal use of
sealants is also likely to remain somewhat dif-
ferent in public health programs than in private
practice. In public programs, sealants should
continue to be highly effective in reducing the
burden of caries in high-risk children. This is
because the children are selected on the basis of
untreated disease and limited access to routine
dental care, and large numbers of children can
be treated under the traditional approach of
sealing large numbers of teeth, including many
that are sound. On the other hand, for patients
who are available for regular care in private
practice, the trend is toward a more selective,
individual approach to sealant use. Here the
decision to treat is made on the basis of the
expected risk for the individual child and tooth
surface, and with the knowledge that sealants
are part of a conservative approach to restora-
tive care. The role of sealants and the related
restorative materials in improving the oral
health of the public is substantial. The chal-
lenge for the practitioner is to be alert for the
inevitable evolution of the recommendations
for the most appropriate use of these materials.
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 28 Diet and Plaque Control
NUTRITION AND ORAL DISEASES
WHAT IS MEANT BY A CARIOGENIC FOOD?
SOFT DRINKS
CONSUMPTION OF SUGARS
CARIOGENICITY OF DIFFERENT SUGARS
Probably more effort has been expended over
the years in trying to prevent caries by dietary
control and toothbrushing than by any other
method. These efforts have been a major part of
traditional dental health education, and they
are aimed at changing personal behavior by
exhorting people to voluntarily restrict their
consumption of sugars and to brush faithfully.
America’s response is to eat more sugar than
ever, although oral hygiene is also probably bet-
ter than ever.
The ingestion of sugars and other highly
refined carbohydrates is a necessary condition
for dental caries to begin (see Chapter 20).
Although mass education to restrict sugar con-
sumption clearly has not worked, restriction of
dietary sugars remains an appropriate part
of the strategy for controlling caries in a caries-
susceptible patient. Development of low- and
noncariogenic sugar substitutes also provides a
few more options for these patients.
Sugars as a risk factor for dental caries were
discussed in Chapter 20. This chapter takes a
critical look at the role of dietary approaches to
preventing oral disease, at the potential for
caries control through the use of sugar substi-
tutes, and at the most appropriate place for oral
hygiene in caries control.
NUTRITION AND ORAL DISEASES
Diet refers to the food and drink that pass
through the mouth, whereas nutrition is
380
NONCARIOGENIC SUGAR SUBSTITUTES
“CLEANSING” AND “PROTECTIVE” FOODS
CARIES CONTROL BY DIETARY
RESTRICTION
PLAQUE CONTROL
concerned with the absorption and metabolism
of nutrients from dietary sources. We stated in
Chapter 20 that there is little evidence to show
that nutritional deficiencies, either during tooth
development or subsequently, cause dental
caries. Similarly, in Chapter 21 we discussed
how periodontitis cannot be treated as a nutri-
tional disorder. Malnourishment is unusual
in the well-fed societies of North America,
although it is occasionally seen among some
who live in deprived circumstances and among
individuals with eating disorders. Where mal-
nutrition is more widespread, as it is in some
low-income countries, there is a potential link
between malnutrition and the oral diseases, as
was discussed in Chapters 20 and 21.
Despite the infrequency of nutritional distur-
bances among North Americans, some well-
meaning dentists have extolled the virtues of
controlling dental caries and periodontal dis-
eases through nutritional counseling. In cases
of rare metabolic diseases that can disrupt
the immune system, oral conditions may be
improved when the patient’s nutritional status
is improved, but in healthy, well-nourished
patients there is no basis for treating existing
dental disease through nutritional (as distinct
from dietary) counseling.
The nutritional status of a patient is rightly
the concern of the attending dental professional,
and all dentists and hygienists should be
sensitive to the signs of nutritional distur-
bances. When a nutritional disturbance or

eating disorder is suspected, referral to a physi-
cian or nutritionist is the correct course of
action. Even when such a patient is treated
successfully for the nutritional problem,
improvement in oral status is likely to follow as
a consequence only in the most severe cases.
WHAT IS MEANT BY A CARIOGENIC
FOOD?
The sugars or other readily fermentable
carbohydrates (Box 28-1) in any food can be
metabolized by cariogenic bacteria in plaque.
Food with this property is termed acidogenic.
Acidogenesis is a necessary, though not suffi-
cient, condition for the development of caries.
The ubiquity of sugars in processed foods
means that a wide range of foods and drinks are
acidogenic. Whether an acidogenic food is cari-
ogenic or not will depend greatly on a number
of factors specific to the individual who eats it,
factors such as predominant bacterial flora,
flow rate and buffering capacity of saliva, fluo-
ride availability, and individual immune fac-
tors. Whether caries develops or not also
depends on how much of the food is eaten and
how frequently it is consumed, whether it is
BOX 28-1 What Are Cariogenic Foods?
Sugars and other fermentable carbohydrates are part of
the etiologic chain in dental caries. The phrase other
fermentable carbohydrates is used a lot in the literature,
and it sounds both broad and vague. What are these
“other fermentable carbohydrates”? The term refers to
the cooked or milled starches in the refined flours used
in making cookies, biscuits, sweet rolls, croissants, and
other processed foods. Their dental significance is that
as simple carbohydrates they can be broken down
further by the salivary enzyme amylase while still in the
mouth and then metabolized by cariogenic bacteria just
as sugars are. For that reason these simple
carbohydrates are considered potentially cariogenic.
Some evidence suggests that starch-sugar mixtures are
more cariogenic than sugars alone.19,20,35,71
Starch is a branched or unbranched polysaccharide
chain of glucose molecules. The term usually refers to
the complex, large-molecule carbohydrates such as
those found in potatoes, broccoli, other fruits and
vegetables, and whole grains. These are all
carbohydrates that have long been viewed as essentially
28 Diet and Plaque Control 381
eaten in isolation or with other foods, and the
nature of any accompanying foods. We there-
fore cannot be certain whether a particular aci-
dogenic food is cariogenic or not for a particular
patient, even if the risk seems high. However, we
can be confident about the converse: because
acidogenesis is a necessary condition for caries,
a nonacidogenic food must also be a noncario-
genic food.
The concept of a cariogenic food was too
broad to be of practical use in caries control,
so attempts were made to determine the cario-
genic potential of a food, defined as the food’s
ability to foster caries in humans under condi-
tions conducive to caries formation.49 The
underlying idea in defining cariogenic potential
was to draw up a rank order of cariogenic foods,
but a 1986 workshop on food cariogenicity
concluded that this approach was unproduc-
tive. Although efforts to identify cariogenic
foods were not followed up because that cate-
gory was so broad, the workshop agreed
that there was value in identifying nonaci-
dogenic foods, which by definition have no car-
iogenic potential.30 Such foods can then be
confidently recommended to patients who
need a sugar-restricted diet.
noncariogenic because they break down very little in the
oral cavity.60,75 These sugars are part of the structure of
fruits, vegetables, and milk, and as such are called
intrinsic sugars. Intrinsic sugars are considered virtually
noncariogenic when eaten in moderate amounts. Added
sugars, sometimes called extrinsic sugars, are held to be
the sugars that are metabolized by cariogenic plaque
bacteria and trigger the events that lead to
demineralization. Some of the literature on this subject
expands the term sugars to nonmilk extrinsic sugars.
There is no important difference in cariogenicity
between refined sugars and brown sugar. Despite the
earlier comment on intrinsic sugars, adherence to a
high-fruit diet does not necessarily protect from
caries.41 However, as an after-school snack, fruits have
considerably more nutritional value than the average
candy bar.
A diet that is generous in vegetables and fruits and is
light in processed food is recognized universally as
compatible with general health. It is also compatible
with dental health.
382 Prevention of Oral Diseases in Public Health
The cariogenic potential of a single food can-
not be satisfactorily tested in human studies
because of the “background noise” from other
uncontrolled consumption of food compo-
nents in a normal mixed diet.24 As one example,
studies to determine whether the consumption
of presweetened breakfast cereals increased
caries incidence were unable to control for
other crucial variables.26 The 1986 workshop
suggested guidelines for testing the cariogenic
potential of foods using a combination of sev-
eral testing regimens, including animal models
and in vitro procedures.30 These protocols were
intended to identify foods with no cariogenic
potential, especially snack foods, but they have
not received much attention.
The Swiss government has been testing the
cariogenic potential of snack foods since 1982
and has permitted snack foods there to be
labeled Zahnfreundlich (which means “tooth-
friendly” and implies nonerosiveness as well) if
they do not lower the pH of interdental plaque
below 5.7 for up to 30 minutes after consump-
tion.48 Under this well-accepted program, tests
of food products are carried out telemetrically
with a plaque electrode. Accepted products are
usually confectionery items sweetened with the
sugar alcohols xylitol, sorbitol, mannitol, or
maltitol, or with Lycasin, a hydrogenated starch
derivative. Fructose does not pass the test.
The impact of this program on the dental
health of the Swiss people is difficult to docu-
ment, however. It is likely to be positive because
a high proportion of Swiss children and adults
have learned to recognize the “tooth-friendly”
logo and to understand that it indicates oral
health benefits.74 The concept has spread to a
number of other countries, including the
United States, where the Food and Drug
Administration (FDA) in 1996 permitted the
claim “does not promote tooth decay” to be
made for sugar-free foods that met specified test
conditions.46
SOFT DRINKS
We noted in Chapter 20 that soft drink con-
sumption is associated with caries and that high
consumption of soft drinks increases the risk of
caries.50 Therefore caries control calls for mod-
est consumption of soft drinks, but in the cur-
rent social environment it is difficult to
promote that message. One obstacle is
America’s insatiable thirst for carbonated soft
drinks and the nonstop advertising that goes
along with it. Even though soft drink consump-
tion has leveled out in the United States over
recent years, it averaged 54.2 gallons per person
in 2002.18 For years all of this sugar consump-
tion was seen as a matter of no concern, but
more recently the high consumption of soft
drinks has been linked with the global obesity
epidemic,67 an epidemic that is well recognized
in the United States. One response to such a
problem should be promotion of good nutri-
tion in infancy, but instead the trend in recent
years has gone the other way, with juices and
soft drinks replacing breast milk, formula, and
cow’s milk. This change generally is not benefi-
cial,68 and too many children are already over-
weight when they begin school. Soft drink
companies have been aggressively marketing
their products by contracting with cash-poor
school districts for the exclusive right to stock
the vending machines in the schools, known as
“pouring rights.” This, too, is a trend that is not
in the public health interest, and it has been vig-
orously opposed by the American Academy of
Pediatrics.4
When we discussed health promotion in
Chapter 5 we talked about the necessity for an
environment in which people could choose
to be healthy. Aggressive marketing of soft
drinks, together with what to a child’s eyes is the
apparent blessing that school districts give to
unrestricted consumption of a particular brand
of soft drink, threatens that environment.
Health professionals in general agree that soft
drinks have little, if any, place in the infant’s diet
and should be consumed only moderately in
later childhood. This is an issue on which it is
logical for dental professionals to join their
medical and public health colleagues in pro-
moting healthy diets for children, for clearly
both dental and general health concerns are
involved.
In view of these issues, it came as a surprise in
2003 when the American Academy of Pediatric
Dentistry (AAPD) received a grant from the
Coca-Cola Company for research into dental
decay.5 Among the concerns raised by this
action, the main one is that this alliance will be
seen as an endorsement of soft drink consump-
tion in early childhood by the AAPD. This

action also puts the AAPD at odds with its med-
ical colleagues in the American Academy of
Pediatrics, which has a clear policy of asking
schools to reconsider these pouring-rights con-
tracts in the interests of children’s health.4 The
AAPD liaison with Coca-Cola also is contrary to
the long-standing policy of the American
Dental Association to oppose promotion of
low-nutrient foods and drinks to children.6
CONSUMPTION OF SUGARS
The material known by the lay term sugar is
sucrose, a disaccharide that is the most com-
mon form of sugar consumed by humans.
Sucrose and other sugars, both monosaccha-
rides and disaccharides, are added to a wide
variety of processed foods; labels on supermar-
ket staples like canned soups, salad dressings,
and processed meats frequently put sugars high
on the list of ingredients. The ingredients on a
label are listed in order of relative proportions,
so the higher on the list an ingredient appears,
the more of it there is in the product.
Consumption of sugars in all forms has con-
tinued to rise in the United States for many
160
Monosaccharides
Sucrose
120
Pounds per capita
80
40
0
1972 1975 1978
Fig. 28-1 Mean annual consumption of total sugars, sucrose, and high-fructose corn syrup plus other monosac-
charides in the United States, 1972-2002.94
28 Diet and Plaque Control 383
years. It exceeded 120 pounds (54.5 kg) per
capita per year in the 1920s8 and has risen
steadily since then. Fig. 28-1 graphs data from
the U.S. Department of Agriculture for 1972-
2002 to show that, although average consump-
tion of all sugars rose steadily over that period,
sucrose consumption declined through 1984
and has leveled out since then. Consumption of
monosaccharides continues to increase. Average
per capita consumption of all sugars in the
United States reached 146.1 pounds (66.4 kg)
in 2002, one of the highest levels of national
consumption in the world. For contrast, some
international values for consumption of sucrose
(not necessarily of total sugars) are shown in
Fig. 28-2. These data do not include the mono-
saccharides that account for more than half of
consumption in the United States, although
monosaccharides are a much smaller fraction of
the sugars consumed in other countries.
Most monosaccharide now consumed in the
United States is high-fructose corn syrup
(HFCS), widely used in place of sucrose in
processed foods and soft drinks. HFCS consists
mostly of fructose, glucose, and other oligosac-
charides. It is used by food manufacturers
1981 1984 1987 1990 1993 1996 1999 2002
Year
384 Prevention of Oral Diseases in Public Health
60
50
40
Sucrose (kg)
30
20
10
0
USA Mexico
Fig. 28-2 Mean annual consumption of sucrose in the United States, Europe, and four other countries in 1996.
(Data are for sucrose only and do not include consumption of high-fructose corn syrup and other monosaccha-
rides.)93
instead of sucrose because it is cheaper and is
produced domestically, so that it is available
from a stable market. Corn is a cheap and abun-
dant crop in the United States. But sucrose has
such a variety of desirable characteristics from
the food manufacturer’s point of view that it is
difficult to replace. Not only does it have a sweet
taste, but sucrose can be baked and boiled with-
out losing its desirable properties of adding
body, luster, and texture to a food product, pro-
moting the emulsification of fats, and acting as
a preservative. When HFCS is used instead of
sucrose in processed foods, the other desirable
qualities of sucrose must come from additives,
the use of which arouses anxiety in many peo-
ple. To complicate the potential health issues,
sucrose can be more harmful to human health
than was once thought because evidence exists
that it contributes directly to the global epi-
demic of obesity.67
A caveat regarding the data in Figs. 28-1 and
28-2 is that they are all “disappearance” data
(i.e., they are derived from the amount of sugar
that is produced and then distributed from stor-
age warehouses). Disappearance data do not
account for industrial use, wastage, and other
losses. Just how much of the “disappeared” sug-
ars actually is consumed by humans is a matter
of speculation, but disappearance figures by
Europe China India Australia
Country or region
themselves most likely overestimate human con-
sumption. Still, these data are collected in the
same way from year to year, so the trends repre-
sented are accurate enough, even if the absolute
amounts should not be taken too literally.
In addition to the considerable shift from
sucrose to HFCS and other syrups in processed
food, two other major changes have taken place
in sugar consumption patterns since the early
twentieth century28:
●
The proportion of energy intake from car-
bohydrate foods has swung from a prepon-
derance obtained from complex starches
(bread, potatoes, whole grain cereals) to a
preponderance obtained from simple car-
bohydrates (principally sugars).
●
The main use of sugars has changed from
discretionary consumption (i.e., from the
sugar bowl on the table) to consumption
by way of processed foods, the “hidden
sugars.” By the mid-1970s, three quarters of
all sugars consumed came from processed
foods.
CARIOGENICITY OF DIFFERENT
SUGARS
Sucrose for years was billed as the “archcrimi-
nal” of dental caries because it was considered

to be so much more cariogenic than other sug-
ars.72 However, later research has suggested that
the differences between sucrose and the various
monosaccharides in terms of cariogenic poten-
tial are less than originally believed.48,59 This is
a difficult issue to study in humans because of
the variability of the human diet, so views are
based principally on extrapolations from ani-
mal studies and laboratory research. One study
in Sweden involving a small number of pre-
school children found that those consuming
invert sugar (a mixture of glucose and fructose)
in place of sucrose had a lower caries increment
over 2 years,36 although the differences did not
reach statistical significance. However, one
could speculate whether America’s reduced
consumption of sucrose (see Fig. 28-1) has
been a factor in the sharp reduction in approxi-
mal and smooth surface caries relative to the
overall caries decline (see Chapter 20). This
speculation is based on the fact that the produc-
tion of extracellular polysaccharides in plaque
depends on sucrose73 and that smooth surface
caries will only develop with plaque that adheres
by means of extracellular polysaccharides.
NONCARIOGENIC SUGAR
SUBSTITUTES
The development of noncaloric sugar sub-
stitutes, marketed for weight control, is big
business in the United States. Commercial
development of these products, from the labo-
ratory to marketing, is time consuming and
expensive. This is mainly because manufactur-
ers must meet stringent FDA requirements for
demonstrated safety before such products go to
market. However, despite the sometimes formi-
dable costs involved, sugar substitutes continue
to be developed. Some, such as the noncaloric
saccharin, have been in common use in the
United States and elsewhere for years.
Aspartame, a dipeptide composed of two natu-
rally occurring amino acids, became available in
the United States in 1982.
Research into the dental applications of
sugar substitutes goes back several decades. The
rationale is that Streptococcus mutans and
Streptococcus sobrinus emerge in plaque flora
when sugar substrate is plentiful but can be sup-
pressed when the diet is low in sugars. A widely
used group of sugar substitutes are the caloric
28 Diet and Plaque Control 385
sweeteners known as the sugar alcohols. The
most commonly used sugar alcohol in the
United States has been sorbitol, which is the
standard sweetener in several “sugarless” chew-
ing gums and over-the-counter medicines. The
advantage of sorbitol over sugars, in terms of
cariogenesis, is that in small amounts it does
not lower the pH of plaque to the point at
which enamel demineralization occurs.21
Sorbitol is considered to have low cariogenicity
rather than to be noncariogenic, however,
because when larger amounts are consumed
both the acid production in plaque and the
number of sorbitol-fermenting microorganisms
can increase.22 Cariogenic microorganisms
“learn” to metabolize sorbitol when their sugar
supply is restricted, a form of adaptation to sor-
bitol that has also been demonstrated in ani-
mals.34 Several clinical trials of sorbitol chewing
gum, however, have shown that these problems
do not occur when consumption levels are low,
around two sticks of gum per day. Use of sor-
bitol gum at this level at least does not promote
caries39 and may help to reverse early deminer-
alization of a lesion.32,58,62
The sugar alcohol that has received most
research attention is xylitol. Xylitol, like other
sugar alcohols, is caloric but has been shown to
be noncariogenic and to possess the properties
of a marketable sweetener. In the late 1960s and
early 1970s, xylitol was the subject of interesting
experiments in the Finnish city of Turku, known
as the Turku sugar studies.86 In the first of the
Turku studies, a small group of volunteer adults
made virtually complete substitution of xylitol
for sucrose in their diets, a change made possi-
ble by having food manufacturers prepare spe-
cial nonsucrose, xylitol-sweetened foods for the
2 years of the study. A second test group con-
sumed fructose-sweetened foods under the
same protocol, and a third group acted as con-
trols by consuming a conventional sucrose-
containing diet. By necessity, this study deviated
from the requirements of an ideal clinical trial
in that the participants were self-selected and
were aware of their group assignment. Still, the
magnitude of the differences among the groups
in new caries experience was impressive. Over 2
years there were practically no new carious
lesions in the xylitol group, whereas there were
more than seven per person in the group eating
the usual sucrose diet and four per person in the
386 Prevention of Oral Diseases in Public Health
fructose-consuming group. Lesions in the adult
test subjects, whose average age was 27.5 years,
were almost all of the “white spot” variety (i.e.,
reversible early demineralization) on smooth
surfaces.84 The quantity of plaque formed in the
xylitol group was also significantly lower.86
In a separate 1-year clinical trial in Turku,
young adult subjects consumed an average of
four sticks a day of xylitol-sweetened chewing
gum, with no other changes in conventional
diet. Control group subjects consumed the same
amount of sucrose-sweetened gum. After a year
the test group subjects averaged 0.3 new DMF
(decayed, missing, or filled) surfaces compared
with nearly 4 surfaces in the sucrose group.85
The lesions were again mostly white spots,
which is why the caries incidence appears high.
Subsequent field trials of xylitol-sweetened
gum and confectionery products have contin-
ued to give impressive results.2,10,52,56 Other
field studies, in one instance with fluoride
added to xylitol gum, have yielded acceptable
positive results only slightly clouded by ques-
tionable study design and data analysis. 15,55,83
In comparisons between sorbitol and xylitol,
xylitol has yielded better results, probably
because of its antibacterial properties.31,37,45
Maternal consumption of xylitol has also been
shown to block the transmission of mutans
streptococci from mother to child.51,88
Xylitol cannot be metabolized by cariogenic
microorganisms16,40 and thus does not reduce
the pH of plaque. The counts of salivary S.
mutans drop as a consequence of consistent use
of xylitol gum, probably because replacement of
sucrose by xylitol in plaque starves the cariogenic
microorganisms. Further analysis of data from
the Turku studies,77,78 in addition to the results
of laboratory studies,87 suggests that xylitol may
promote remineralization, and there are also
reports that xylitol can arrest established dentin
caries.66 This evidence has led to the possibility
that xylitol may be more than noncariogenic and
may actually be therapeutic or anticariogenic.
Although these claims require further confirma-
tion before they can be accepted, research sup-
ports the conclusion that even partial
substitution of xylitol for sucrose, such as in con-
fectionery products, is an effective means of
caries prevention at the public health level.82
In terms of general health consequences,
some of the earlier xylitol studies reported some
mild laxative effects in some study participants,
but this was not reported in more recent trials
when lower dosages were used. Xylitol has been
approved for “special dietary use” in the United
States since 1963, although it remains hard to
find in chewing gums and other snack products.
Xylitol is much more expensive than sucrose,
however, and because it is destroyed by heat it
cannot be used in cooked food products. Thus
its use may be restricted to products such as
chewing gum that require only small amounts
of sweetener. With the FDA’s acceptance of the
“tooth-friendly” logo,46 it is hoped that more
xylitol-sweetened products will be seen in the
United States. Currently xylitol is much more
common in chewing gum in Canada and
Europe.
“CLEANSING” AND “PROTECTIVE”
FOODS
As discussed in Chapter 20, long-held and stren-
uously asserted beliefs about the anticariogenic
properties of “cleansing” foods have little sub-
stance. The thinking here was that chewing a
fibrous food (apple, carrot, celery) would clean
plaque from tooth surfaces and thus prevent
caries; however, research has long since shown
that chewing fibrous foods does not remove
plaque. Of course, there is obvious nutritional
merit in snacking on fresh fruits and vegetables
rather than on candy bars: more fiber, more vita-
mins and minerals, less fat. But unless the sugar
intake of persons eating fibrous snacks is drasti-
cally reduced in addition, which as stated earlier
is difficult to do without a radical move away
from processed foods, the impact on caries will
be minimal. Even that very symbol of oral
health, the apple, has been shown to lower
plaque pH soon after ingestion38 and to induce
caries in rats when eaten ad libitum.91
One food with reported protective factors is
cheese; there is evidence in humans to show
that finishing a meal with cheese reduces the
acidity of plaque79 and therefore presumably its
cariogenicity. Animal studies, which of course
can be more tightly controlled than studies in
humans, support this finding.61
In addition to fluoride, other dietary trace
elements have been associated with caries expe-
rience: molybdenum with low disease levels81
and selenium with high levels.43 However,

evidence for an important etiologic role is weak,
and these reports have no practical implications
for caries control. Among the various food addi-
tives intended to reduce the carious attack,
phosphates have probably received most atten-
tion. In numerous animal studies phosphates
have been shown to reduce caries when added
to the diet, but studies in humans have yielded
disappointing results.54,63 The reductions in
caries have been too small to be of any signifi-
cance, and the phosphate tends to give the food
an unpleasant taste.
Nutritious and fibrous foods are naturally to
be recommended for good general health.
Although the impact on oral health of a bal-
anced diet high in unprocessed foods can only
be good, it cannot be demonstrated under mod-
ern conditions of fluoride exposure that such a
diet, by itself, will improve oral health status.
Nor is there any evidence to support chewing of
carrots, celery, or apples as a means of cleaning
plaque from teeth. This form of dietary counsel-
ing should not become the centerpiece of den-
tal health education, although dental personnel
should always encourage healthy food choices
by their patients.
CARIES CONTROL BY DIETARY
RESTRICTION
A dietary regimen that involved strict control of
carbohydrate intake was developed for caries
control in the immediately prefluoride years.53
Success was based on reducing counts of Lacto-
bacillus acidophilus, and this regimen demanded
almost total abstinence from all forms of carbo-
hydrate for a short period, with a gradual return
to limited carbohydrate intake. This draconian
regimen of dietary control was too much for
most patients, however, and it had little broad-
scale success. Of more concern in today’s world,
drastic reduction of all forms of carbohydrate,
which include fruits and vegetables, is clearly
unwise because it could lead either to excessive
intake of fat and protein or to energy depriva-
tion. Dietary guidelines from the U.S. Depart-
ment of Agriculture urge the consumption of
more unrefined carbohydrates (e.g., fruits, veg-
etables, and whole grains) but retain the recom-
mendation for restrained consumption of
refined carbohydrates (sugars and other fer-
mentable carbohydrates).92
28 Diet and Plaque Control 387
In Chapter 20 we discussed how the Vipe-
hölm study42 influenced dental health educa-
tion and how application of the results of that
landmark study may have become misdirected.
In normal-living populations, there is no epi-
demiologic evidence that consumption of
sticky foods is more strongly associated with
caries experience than is consumption of sug-
ared drinks, although this conclusion depends
on the quantities consumed (i.e., food cario-
genicity rather than cariogenic potential).
Sugared rinses served very well to demonstrate
the Stephan curve, the first laboratory demon-
stration that ingestion of sugars caused an
immediate sharp drop in plaque pH, followed
by a gradual return to normal pH due to salivary
buffering action.90 The Stephan curve is shown
in Fig. 28-3. Sugared rinses were also the basis
of experimental caries studies in humans,96 so
advice to “take your sugars in drinks rather than
sticky foods” can hardly be recommended given
this evidence. Another aspect of this subject is
that consumer perceptions of “sticky” foods are
poorly related to objective measures of food
retention.57
We also discussed in Chapter 20 how pro-
spective studies in the 1980s could not demon-
strate a relationship between caries experience
and frequency of eating among children, and
that the conclusion of the Vipehölm study on
the importance of frequency of consumption
may have been based on a distorted eating pat-
tern that is rarely seen in the general popula-
tion. Health educators today are advised to
concentrate on reducing total intake of sugars
by caries-susceptible people rather than to
focus on “sticky” foods or details of snacking
frequency.
Research studies in humans have identified
many people who get little caries even though
they consume a lot of sugars25,80; extensive
dietary counseling for such individuals is clearly
not time well spent. The philosophy behind
extensive effort to obtain major reductions in
such individuals’ consumption of sugars to
prevent a small amount of disease must be
seriously questioned. Patients who are more
susceptible to caries, however, can benefit con-
siderably. Therefore extensive dietary counsel-
ing in the dental office should be concentrated
on patients who show an obvious susceptibility
to caries.
388 Prevention of Oral Diseases in Public Health
8.0
6.0
Sucrose rinse
Plaque pH
4.0
2.0
0
0 5
Minutes after rinse
Fig. 28-3 Data from Stephan’s experiments showing the Stephan curve. In the group using the sucrose rinse, a
sharp and immediate drop in plaque pH was seen; in the control group using a water rinse, no change occurred.90
On a community level, dietary advice in den-
tal health education should be linked with gen-
eral efforts to educate the public regarding wise
food choices for healthy living and judicious
use of the national dietary guidelines. High-
sugar foods are often high-fat foods as well, so
dentally oriented advice is completely in har-
mony with broad advice to enhance the public
health. Drastic reductions in sugar consump-
tion, even if feasible in the United States, may or
may not have much impact on caries levels but
would likely lead to replacement of lost energy
by consumption of fat.27 This would clearly not
be a move to enhance the public health.
PLAQUE CONTROL
Dietary restriction has historically been used in
conjunction with frequent plaque removal to
prevent caries. From the time of Miller in the
1880s, caries was seen as theoretically preventa-
ble by regular and careful oral hygiene proce-
dures to remove plaque. Countless hours of
dental health education have been devoted to
promoting that end, based on the adage that “a
clean tooth never decays.” This approach to
controlling caries by focusing on oral hygiene is
based on the “nonspecific plaque hypothesis,”
which in turn was based on the incorrect
assumption that all bacteria in plaque are of
Water rinse
10 15 20 25 30
equal cariogenicity and should therefore be
removed. It also stems from the pioneering
work of Stephan in the 1940s (see Fig. 28-3),
which quickly became the basis for dental
health education aimed at promoting brushing
immediately after eating to neutralize the
impact of “acid attacks.”
Even with all the knowledge gained from
modern research, however, the relation between
caries incidence and level of oral hygiene can
still be confusing. Plaque harbors cariogenic
and periodontopathogenic bacteria, but it also
is the main intraoral repository of fluoride and
other remineralizing substances. Presumably
the human race evolved plaque for some bene-
ficial purpose, although one would doubt it
from the message given out by most dental
health education materials.
Despite historically mixed research evidence
linking oral hygiene to caries incidence,7,17,69
interest in stringent oral hygiene was piqued by
a series of reports in the 1970s which concluded
that caries incidence in children could be virtu-
ally eliminated by meticulous plaque removal
carried out by trained dental auxiliaries at fre-
quent intervals.11-13,64 These reports are known
collectively as the Karlstad studies after the
Swedish county in which they were conducted.
Intervals between professional cleanings were
2 weeks in younger children, whereas in older

children spectacular results were maintained
when the time between cleanings was extended
to 8 weeks after an initial 2 years at 2-week inter-
vals.65 The procedures involved in the profes-
sional cleaning of children’s teeth are detailed
in Chapter 29.
Benefits of this protocol probably came from
a combination of (1) plaque control, (2) inten-
sive use of topical fluoride paste, and (3) dental
health education and oral hygiene practices at
home, although the researchers concluded that
most benefit came from the oral hygiene proce-
dures.12 Caries reductions of 98% were reported
over 2 years,11 although attempts by others to
replicate the Karlstad regimen were not able
to achieve the same level of success.1,9,14,44
More recently, studies on the Danish island of
Bornholm have reported great caries-preventive
success through rigorous control of plaque
deposits on erupting first molars.29 Like the
Karlstad regimen, the Bornholm approach is
resource intensive, so much so that it is of
doubtful utility in places that do not have
Scandinavian-level resources in a school dental
services.
Studies carried out by Scandinavian researchers
with small groups of children continue to
relate good oral hygiene to low caries experi-
ence.3,23,47,70 Poor oral hygiene is also a clear
risk factor for root caries in older people.89,95
On the other hand, despite extensive improve-
ments in the caries status of Quebec children
between 1977 and 1990, no improvement in
oral hygiene could be found,76 and oral hygiene
levels were not associated with the progression
of white spots to dentinal lesions.33 Even if a
poor level of oral hygiene does promote caries,
extensive professional care to clean up a dirty
mouth may not be time well spent if the under-
lying reasons for poor oral hygiene are not
addressed.
Good oral hygiene is so clearly a desirable
goal for social and periodontal reasons (see
Chapter 29) that education or treatment to
achieve it cannot be simply dismissed. The ques-
tion, however, is one of cost effectiveness, of the
best use of a professional’s time. The intensity of
the Karlstad protocol, in education and home
care as well as in the professional treatments
themselves, demands a high investment in
equipment and personnel and absorbs some 3
hours of chair time per child each year.9 The cost
28 Diet and Plaque Control 389
of the Karlstad approach therefore makes it
unrealistic for most public services; caries pre-
vention efforts are far better channeled into fluo-
ride and sealant programs. The main purpose of
regular toothbrushing, in terms of caries preven-
tion, is to introduce fluoride into the mouth reg-
ularly via the toothpaste. The plaque-removal
effect appears secondary in caries prevention,
although it can have primary benefits in control-
ling gingivitis (see Chapter 29). Regular tooth-
brushing with a fluoride toothpaste should be
encouraged as a regular daily routine for all peo-
ple, whether susceptible to caries or not.
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 29 Prevention of Periodontal Diseases
RATIONALE FOR PLAQUE CONTROL
NATURE OF DENTAL PLAQUE
APPROACHES TO PLAQUE CONTROL
MECHANICAL PLAQUE REMOVAL
BY THE INDIVIDUAL
Frequency of Toothbrushing
Type of Toothbrush
Toothbrushing Methods
Interdental Cleaning
Individual Motivation
MECHANICAL PLAQUE REMOVAL BY THE
DENTAL PROFESSIONAL
Although our understanding of periodontal
conditions is growing rapidly (see Chapter 21),
prevention and control of periodontal con-
ditions still must be based on the periodic
removal of plaque and calculus, whether by the
individual or by a dental professional. There is
no parallel in prevention of periodontal dis-
eases to a public health measure such as water
fluoridation.
Our current understanding that only some
5%-15% of the population suffers from serious
periodontitis has led some to downplay the
importance of prevention; this is the view that
“periodontal disease doesn’t matter anymore.”
This view is clearly faulty, because this level
of prevalence still means that some 30 million
Americans suffer from serious periodontitis.
Based on the data given in Chapter 21, eight
times that number have moderate adult perio-
dontitis, much of which requires treatment and
could probably be prevented. Prevention of
periodontitis still is clearly a worthwhile public
health endeavor; the problems and the frustra-
tions come with our limitations in how to
accomplish it. Even though our understanding
of periodontitis has expanded greatly over
recent years, the only practical approach to pre-
Karlstad Studies
Prophylactic Treatment for Adults
PROFESSIONAL PLUS PERSONAL CARE
CHEMOTHERAPEUTIC METHODS OF PLAQUE
CONTROL
Chlorhexidine
Other Antibacterial Compounds
Anticalculus (“Tartar-Control”) Toothpastes
COMMUNITY-BASED CONTROL
OF PERIODONTAL DISEASES
vention of periodontitis (as opposed to its con-
trol through clinical treatment) is to prevent
and control gingivitis.
RATIONALE FOR PLAQUE CONTROL
The rationale for controlling periodontal condi-
tions by regular plaque removal is based on the
premise that supragingival plaque, if undis-
turbed, will become subgingival plaque,92 and
subgingival plaque has the potential to be colo-
nized by periodontopathogenic bacteria.
Although relatively few gingivitis sites progress
to periodontitis (see Chapter 21), we still can-
not identify those sites that will. Accordingly,
the principle for prevention has not changed for
years: the regular and consistent control of
plaque buildup, supragingival and subgingival,
soft and mineralized (calculus), on the teeth
and in the gingival crevices. This approach is
bacteriologically nonspecific, for it seeks to con-
trol the buildup of all plaque. It also depends
strongly on individual motivation for success.
Plaque control is therefore unlikely ever to be
completely effective in preventing periodontal
diseases in a population, although individual
success is common. Until research produces
393
394 Prevention of Oral Diseases in Public Health
methods of controlling periodontal infection,
enhancing host response, and identifying sus-
ceptible individuals, however, mass plaque con-
trol by personal, professional, or chemical
means is the best we can do.
This chapter deals with methods for control-
ling the deposition of dental plaque, an
approach that can effectively prevent gingivitis.
As was detailed in Chapter 21, however, the role
of plaque in periodontitis is not so straightfor-
ward. Plaque deposits may be a necessary con-
dition for periodontitis, but clearly they are not
sufficient. In other words, susceptible people
may have to be stringent about oral hygiene, but
there are millions of people with poor oral
hygiene who do not have serious periodontitis.
There is an analogy here with the role of con-
sumption of sugars in the development of
caries: caries-susceptible persons have to restrict
their intake of sugars, but there are many people
who consume a lot of sugars but have little or
no caries as a consequence.
NATURE OF DENTAL PLAQUE
Although dental plaque is commonly depicted
as the root cause of both caries and periodonti-
tis, one should remember that it must have
evolved in humans for some purpose.
Commercial advertising would have us believe
that oral health depends on the complete
removal of all plaque at all times, but clearly that
is not only not possible but also not desirable.
Dental plaque forms naturally on the teeth and
benefits the host by helping to prevent intraoral
colonization by exogenous species.88 Plaque’s
role in promoting remineralization of deminer-
alized lesions was described in Chapter 20.
Dental plaque is a natural biofilm that forms
on the tooth surface and consists of a diverse
microbial community embedded in a polymer
matrix of bacterial and salivary origin.89 After a
tooth surface is cleaned, the pellicle, a condi-
tioning film of proteins and glycoproteins, is
adsorbed rapidly onto the tooth surface. The
interactions between pellicle and early bacterial
colonizers are the first steps in plaque forma-
tion. Secondary bacterial colonizers adhere to
these early colonizers through specific molecu-
lar interactions, a process that contributes to the
pattern of bacterial succession. The biofilm
character of plaque allows the survival of a
diverse bacterial flora.24 Although microbial
adhesion is how plaque formation begins,
microbial multiplication is thought to be the
dominant factor in the buildup of dental
plaque, and the nature of this microbial prolif-
eration is highly dependent on the local envi-
ronment. Because environmental conditions
vary from place to place within the oral cavity,
each site with plaque represents its own distinct
ecosystem, and the dominant microbial com-
position at the site depends on the outcome of
numerous host-microbe and microbe-microbe
interactions.106
The clinical picture of all this activity has
been well described. After plaque has been com-
pletely removed, it re-forms slowly on the
supragingival tooth surface for about 3 days,
and then if left undisturbed it increases rapidly
to reach a maximum bulk after 7 days. The vari-
ous microbial interactions actually keep the
bacterial composition of plaque relatively sta-
ble, but when this homeostasis breaks down,
the shifts in microbial balance can set up con-
ditions for caries or gingivitis to begin. Plaque
accumulation around the gingival margin
leads to an inflammatory host response and an
increased flow of gingival crevicular fluid.88 Few
bacteria can be isolated from around healthy
gingival tissue, although with gingivitis there
is a considerable increase in the numbers
and complexity of bacteria as the lesion devel-
ops.92 Subgingival plaque microflora shift from
being predominantly gram positive to includ-
ing increased levels of anaerobic gram-negative
organisms; the character of subgingival plaque
is thus quite different from that of supragingival
plaque. Specifically, the gram-negative anaer-
obes Porphyromonas gingivalis and Bacteroides
forsythus in subgingival plaque have been associ-
ated with both loss of periodontal attachment
and bone loss.48,49 Frequent professional
supragingival cleaning, added to good personal
oral hygiene, has a beneficial effect with regard
to subgingival microbiota in moderately deep
pockets.54,120 Subgingival plaque is also char-
acterized by oral spirochetes, whose role in
periodontitis is still not clear, although their
presence in the subgingival plaque is seen as a
marker for disease.118
Calculus was formerly viewed only as an
“irritating factor” in the development of peri-
odontitis64 and did not get much research

attention. Today, however, calculus is recog-
nized as a calcified matrix that can harbor peri-
odontopathogenic bacteria, and subgingival
calculus is closely associated with gingivitis and
periodontitis.33 Therefore, the initial formation
and continued presence of both supragingival
and subgingival calculus are to be prevented to
the extent possible. The only known method is
to control the initial formation of supragingival
plaque and calculus.
APPROACHES TO PLAQUE CONTROL
Because plaque has some identifiable health
functions and because disease comes more
from an upset in the homeostatic balance than
from infection with exogenous organisms, dis-
ease prevention should be geared more toward
plaque control than plaque eradication. This
concept is referred to as the ecologic plaque
hypothesis.87 The goal in preventing periodonti-
tis is to prevent fresh plaque from becoming
established plaque, which permits the growth of
specific periodontopathogenic bacteria,102,123
and to prevent supragingival plaque from
becoming established subgingivally.
Several approaches to plaque control can be
quickly ruled out as having no scientific basis:
rinsing with water and chewing a fibrous food
(e.g., remove loose food debris but do not affect
plaque). There is no evidence to alter the long-
held view that preventive benefits cannot be
achieved by changes in diet or nutrition,74,110
although, given the importance of the host
response in periodontitis and the fact that nutri-
tion is a vital part of the immune reaction, the
role of nutrition in periodontitis should con-
tinue to be studied.
Primary prevention of gingivitis requires
consistent, thorough control of plaque accumu-
lation on a lifetime basis. The rationale is to pre-
vent plaque from reaching the stage of maturity
at which gingivitis begins. Some people are
capable of maintaining an adequate oral
hygiene status largely by their own efforts, but
many are not. The dental professional will con-
sistently see some level of gingivitis in the latter
patients and may become frustrated in the effort
to eliminate gingivitis entirely. For these
patients, the dental professional’s goal should
be to maintain the gingivitis at as low a level as
possible. As long as the lowest possible level of
29 Prevention of Periodontal Diseases 395
gingivitis can be maintained over time, subse-
quent loss of periodontal support is likely to be
minimized. This is true for the majority of
patients who are at low risk of severe periodon-
titis. It is less the case for those patients with
aggressive periodontitis who fit the compro-
mised host model described in Chapter 21.
Prevention of disease in these patients is diffi-
cult because we do not yet have the means of
influencing the deficient host response to a
periodontal challenge.
As long as plaque accumulation remains
supragingival, it can be controlled by mechani-
cal or chemotherapeutic means.101 Once
plaque becomes established subgingivally,
however, the individual patient cannot remove
it by self-care, and professional intervention is
necessary. The goal of prevention of periodon-
tal conditions through plaque control by the
individual is to keep supragingival plaque from
accumulating.
There are essentially three approaches to pre-
venting the build-up of dental plaque, each of
which is assessed in turn. They are:
●
Mechanical plaque removal by the
individual
●
Mechanical plaque removal by the dental
professional
●
Chemotherapeutic methods of plaque
control
MECHANICAL PLAQUE REMOVAL
BY THE INDIVIDUAL
Self-care is a fundamental part of periodontal
health. Unless the individual is able to main-
tain at least a reasonable level of oral cleanliness
by regular and consistent home care, the bene-
fits of treatment by dental professionals will be
limited. Individual effort means mechanical
plaque removal with a toothbrush and aids
such as dental floss, an interproximal brush,
and wood points.
Although individual oral hygiene practices
are fundamental to the promotion of oral
health, it is surprising how little is really known
about such basic things as the most efficient
type of toothbrush and how often the teeth
should be brushed. Research studies in these
areas have often been run for only short periods
and with atypical populations, such as dental or
dental hygiene students. Long-term effects and
396 Prevention of Oral Diseases in Public Health
the validity of projecting results to the general
population are thus difficult to assess.
Frequency of Toothbrushing
The limited information that is available indi-
cates that a thorough oral cleansing should be
carried out at 24- to 48-hour intervals.61,66
Considering the time needed for plaque to
mature bacteriologically, brushing after every
meal, which was usually impractical anyway, is
unnecessary to prevent gingivitis. But because
toothbrushing with a fluoride toothpaste is also
a major source of fluoride exposure for caries
prevention, it is best carried out at least twice per
day to maintain oral health. Brushing in the
morning and evening fits with most peoples’
daily routines and should be the basis for educa-
tion of the public and dental patients. Of course,
patients who have received treatment for peri-
odontitis are likely to be at high risk for further
disease, and more stringent home care regimens
may be required for them.120
Type of Toothbrush
Little research has been carried out on the best
type of toothbrush; what evidence there is sug-
gests that it really does not matter much.
Children clearly should use a smaller brush,
and the dentist or hygienist may want to recom-
mend different sizes and degrees of softness,
depending on each patient’s manual dexterity,
enthusiasm, and oral health. Soft brushes gen-
erally are preferred to minimize gingival dam-
age with enthusiastic brushing. Manufacturers
are constantly coming out with new designs,
so anyone can find a toothbrush that is com-
fortable and efficient. However, these recom-
mendations are based on common sense rather
than on firm evidence.
Electric toothbrushes with a rotary action
have been found to be more effective plaque
removers in closely supervised clinical trials,117
although it is uncertain how well these findings
reflect everyday effectiveness. Both manual and
power-driven toothbrushes are effective if used
properly; differences between individuals’
brushing efficiency are likely to be much greater
than inherent differences between types of
toothbrushes. New versions of power-driven
brushes are constantly being marketed, some
with heavy advertising, and most have not been
subjected to rigorous testing. Power brushes
may be particularly useful for handicapped per-
sons or others with low manual dexterity.
Toothbrushing Methods
A variety of toothbrushing methods, some
requiring a lot of manual gymnastics, have been
described in the dental literature down the
years. Proponents of one method or another
have traditionally been vehement in the defense
of their method’s efficacy, a good example of
the rule that the level of passion that people
have about an issue is inversely proportional to
its scientific basis. In fact there is little difference
between the various methods in their ability to
remove dental plaque.42,52,100,103 From these
studies, limited though some of them are, the
scrub method emerges as the simplest tech-
nique available and one that is no less effective
than any other. It requires minimal manual dex-
terity and patient concentration, and generally
seems best for most persons.
Interdental Cleaning
The rationale for supplementing toothbrushing
with use of dental floss, interdental brushes, or
wood points to clean below the contact areas is
that even assiduous use of the toothbrush usu-
ally cannot penetrate these areas efficiently.
There is some limited evidence that interdental
cleaning, by floss or interdental brushes,
reduces interdental gingivitis and plaque more
than toothbrushing alone.27,78
Many dental health education materials
extol the efficacy of dental floss: “brush and
floss” long ago replaced the exhortation to just
“brush.” There is still little evidence, however, to
show that flossing, as practiced by the individ-
ual with normal interdental spaces, adds much
to the efficiency of brushing,55,100,107 nor are the
limited research studies able to find a difference
between waxed and unwaxed floss in cleaning
efficiency.22,30,40,78 In cases in which papillae
have diminished to leave open interdental
spaces, interdental brushes are superior to
floss.23,32 Many people prefer wood points to
floss because floss can break and become stuck
in awkward contact areas, and wood points can
be effective interdental cleaners.
Individual Motivation
The individual practice of regular, thorough,
and consistent oral hygiene procedures depends

largely on the interest of the individual in his or
her oral health. Dentally conscious people
have this interest already, but many others
do not. Oral hygiene practices must fit into
the lifestyle of each individual, and lifestyles are
rarely changed by exhortation. To illustrate the
lifestyle issue, a British study found that school-
children who reported more frequent tooth-
brushing also reported more frequent bathing,
use of deodorant, and hand washing after visit-
ing the toilet.85 Information like this comes as
no surprise.
Knowledge is usually thought to pre-
cede action, although a study of periodontal
patients in North Carolina found poor correla-
tion between knowledge of the disease process
and periodontal health.16 Carefully thought-
out and well-organized motivational programs
aimed at schoolchildren have produced poor
results in the United States.53,56 A typical find-
ing came from a study of supervised daily
toothbrushing by schoolchildren in Sweden:
gingivitis was reduced for the duration of the
program, but the improvement disappeared
when the supervision ended.70,71 Although
compliance with periodontitis treatment
instructions is related to health beliefs,65 the
effects of individual chairside instruction are
usually weak.115,122 Doubts are thus raised
about what motivational programs really do;
they may succeed only in reinforcing existing
favorable attitudes and not in altering negative
ones. 90 A Danish longitudinal study found
that oral hygiene behavior in youth was found
to predict periodontal health in adulthood,73 a
finding which confirms that attitudes and oral
health behavior are principally determined by
factors outside the dental office. (Issues in
health promotion are discussed more fully in
Chapter 5.)
For dental professionals who try to induce
individual patients to improve their daily
oral hygiene performance, greatest success
may come from a personal and common
sense approach by the dentist or hygienist.
Some patients will respond better than others.
Objective monitoring by measurement of gin-
gival bleeding, pocket depth, periodontal
attachment levels, calculus deposits, and plaque
is important because subjective impressions of
progress can be misleading. Reinforcement of
simple messages and constant encouragement
29 Prevention of Periodontal Diseases 397
of the individual’s efforts seem to be important
factors. Oral health professionals must work
within the limitations of the individual patient,
and within their own limitations too.
Oral hygiene in the United States is consid-
ered by most experts to be constantly improv-
ing, a trend thought to result from heightened
awareness, heavy advertising, and constantly
improving oral hygiene products. Public health
education programs intended to produce mass
improvement in oral hygiene have had little
measurable impact on this trend.43,53 Time
given to this form of education in public health
programs, especially in populations bom-
barded by television commercials about oral
hygiene, could probably be much better spent
on primary prevention or on providing dental
care to needy people. This may not be the case,
however, in a low-income country, where basic
knowledge of oral hygiene may be lacking.
“Toothbrush drills” are quite properly a com-
mon part of dental public health education in
such countries, whereas they may be unneces-
sary in high-income nations.
MECHANICAL PLAQUE REMOVAL
BY THE DENTAL PROFESSIONAL
Professional care is necessary to remove subgin-
gival plaque and calculus; the patient cannot
remove plaque from deep pockets. The benefits
of professional plaque removal have been
shown in studies of children and adults who
were in reasonable periodontal health to begin
with, as well as in studies of adults receiving
treatment for advanced disease.
Karlstad Studies
The discussion of the Karlstad studies in
Chapter 28 was related principally to caries; this
section discusses the studies in relation to peri-
odontal diseases. Among children, spectacular
success in preventing gingivitis was reported by
the Axelsson-Lindhe group in their investiga-
tions in Karlstad, Sweden.10,11,13,69 Studying
children ages 7-14 years, this research group
set out to show that a regimen of intensive pro-
phylactic procedures that went considerably
beyond routine prophylaxis would be effective
in preventing both caries and gingivitis. The
detailed protocol for the Karlstad regimen is
given in Box 29-1.
398 Prevention of Oral Diseases in Public Health
BOX 29-1 Protocol for the Oral Cleaning Carried
Out in the Children Ages 7-14 Who Participated
in the Karlstad Studies10,69
●
Detailed initial explanations of oral disease etiology
and purpose of treatment by the dentist or auxiliary
carrying out the treatment. Involvement of the family
was considered integral to the program’s success.
●
Identification of plaque in the patient’s mouth by
disclosing tablet, then demonstration of correct
toothbrushing technique for removing the stain. The
patient then used dental floss under supervision.
These oral hygiene instructions were repeated
throughout the course of treatment as necessary.
●
Rubber cup cleaning of accessible surfaces and use
of engine-mounted pointed bristle to clean fissures
in occlusal surfaces. A fluoride-containing
prophylactic paste was used for these procedures.
●
Interdental cleaning, again by the dentist or auxiliary
providing the treatment, with dental floss and
reciprocating interproximal tips. Again, the
fluoridated prophylactic paste was forced
interdentally and kept in close contact with the
proximal surfaces by the floss and the tips.
These procedures were carried out by professionals
every 2 weeks over a 2-year period. In the third year,
the time between these “professional cleanings,” as
the Karlstad researchers called them, was extended to
4 weeks for the 7- to 11-year-olds and to 8 weeks for
the 13- to 14-year-olds. The continuing good results
with this reduced frequency of cleaning was attributed
to the background effects of the first 2 years. These
researchers were firm in their contention that
professional cleanings five to eight times per year are
still not enough by themselves to control gingivitis.
Other European groups who carried out
studies using the Karlstad protocols also
achieved good results, although none of them
quite reached the Karlstad heights.1,7,17,62 A
British study followed up its participants a year
after the study ended, and it is probably not sur-
prising that the 3-year reduction in plaque mass
of 54% had by then declined to 26%.8
No studies of the Karlstad regimen have been
carried out in the United States or Canada
because the expense of this personnel-intensive
regimen is beyond the capacity of public health
agencies. In addition, the implied paternalism
of the regimen probably cuts against the North
American cultural grain of individualism. One
study in the United States found that perform-
ing prophylactic procedures twice per year in
children ages 10-11 produced neither beneficial
reductions in gingivitis nor improvements in
oral hygiene levels,99 although this schedule is
much less intense than the Karlstad regimen.
Another study of a Karlstad-type regimen in
young Brazilians found that the intensive
preventive care did not slow down the progres-
sion of periodontitis when compared to either
routine oral hygiene instruction or to no
instruction.3 The authors speculated that they
may have been dealing with a compromised
host type of periodontitis (see Chapter 21).
Periodontitis would not be expected to respond
much to even intensive oral hygiene if the cause
lies in a deficient host response, whereas peri-
odontitis caused by local factors would show a
response.
Prophylactic Treatment for Adults
Routine prophylactic care of nondiseased adults
is discussed here, rather than the treatment of
patients with periodontitis, which is a different
issue. Patients, by definition, are either suscepti-
ble to periodontitis or not, so all clinical studies
showing the value of maintenance prophylactic
care in treated patients are carried out in suscep-
tible populations.96,97
Studies that examined the value of routine
prophylaxis in adult populations in the com-
munity (i.e., in adults who were not patients)
are now many years old. Qualified success from
routine prophylactic treatments in adults (on a
less intense schedule than the Karlstad regimen)
was reported in Norway.84 For 5 years factory
workers received a prophylactic treatment
plus oral hygiene instruction at 6-month inter-
vals, or at 3-month intervals for “more severely
affected” individuals. The greatest benefits were
gained by persons whose oral hygiene status
was best to begin with, and least success was
achieved among those with initially poor oral
hygiene. This difference in results emphasizes
the importance of self-care and the limitations
of professional cleaning without it.
In Axelsson and Lindhe’s study of adults in
Karlstad over 15 years, the professional clean-
ings were carried out every 2-3 months for the
first 6 years, and one or two times per year for
a subsequent 9 years for most participants.14

A small subgroup of persons who had devel-
oped caries or further loss of attachment during
the study were retained on a more intensive
professional cleaning regimen for the entire 15
years. All participants exhibited almost no fur-
ther loss of periodontal attachment during this
period. In line with the philosophy of these
researchers, intensive oral hygiene instruction
for self-care accompanied the professional
cleanings. The authors concluded that self-per-
formed oral hygiene (with a fluoride toothpaste
of course) together with a stringent regimen of
professional treatment maintained oral health.
The stringency of the regimen was increased
for patients considered to be at greater risk for
periodontitis.
In the United States a study involving office
workers in California found that a professional
prophylactic treatment plus intensive oral
hygiene instruction every 2-4 months reduced
levels of plaque and gingivitis relative to a con-
trol group and greatly slowed the rate of loss of
attachment.111 A separate study of young men
found a tendency toward improved gingival
health accompanying greater frequency of pro-
phylactic procedures, although differences
resulting from prophylactic treatments at
12-month, 6-month, and 4-month intervals
were not pronounced.113 An Air Force study68
found that beneficial results were proportional
to the frequency of the prophylactic treatment
received; best results were achieved in the group
that received four prophylactic treatments per
year plus oral hygiene instruction at each
appointment. None of these American studies
achieved Karlstad-type results, but they did not
test nearly so intensive a regimen. Collectively,
they demonstrated modest across-the-board
results. In light of our current views, it would
have been helpful if the authors had reported
their results in terms of distributional patterns;
it is likely that, as other similar studies have
shown, best results were achieved in those
patients who were best motivated to begin with.
PROFESSIONAL PLUS PERSONAL
CARE
The studies just described have some limita-
tions, but collectively they indicate that profes-
sional prophylactic treatment can help with
plaque control in many people. It must be
29 Prevention of Periodontal Diseases 399
reemphasized, however, that the best results
were obtained when excellent personal oral
hygiene status was maintained by the individ-
ual, which raises questions about the value of
regular professional prophylactic treatments for
periodontally healthy adults with good oral
hygiene.
The conclusions from these studies suggest
that a thorough professional prophylactic pro-
cedure at 2- to 4-month intervals (longer in
some patients), combined with a high level of
individual oral hygiene, is enough to prevent
the destructive periodontal disease that leads to
tooth loss. It might also be overtreatment.
Whether the same results could be achieved in
periodontally healthy adults without the pro-
fessional intervention is an open question.
Questions also arise in view of the epidemio-
logic studies in untreated populations (see
Chapter 21), which show that some people with
virtually no oral hygiene practices, and hence
extensive gingivitis, develop little serious peri-
odontitis. It could be concluded that persons
susceptible to periodontitis may need frequent
professional maintenance care, but the need for
such care for nonsusceptible persons is by no
means so clear.
CHEMOTHERAPEUTIC METHODS
OF PLAQUE CONTROL
The inability of many persons to remove their
own dental plaque consistently results from
insufficient knowledge, poor mechanical dex-
terity, or lack of opportunity or motivation. The
idea of a chemical method of plaque removal, a
mouthrinse or toothpaste that does it all, is
therefore highly attractive. Research over many
years has led to the development of products
that show some plaque-control success in spe-
cific circumstances. Commercial competition in
the marketing of plaque-preventive products is
keen, so much so that the American Dental
Association (ADA) has established guidelines
for conducting clinical trials of products claim-
ing to control plaque to support their accept-
ance by the Council on Dental Therapeutics.4
These guidelines are listed in Box 29-2, and they
conform well to the requirements of acceptable
clinical trials given in Chapter 13. If consistently
applied, they will serve professionals as well as
the public in their choice of both prescription
400 Prevention of Oral Diseases in Public Health
BOX 29-2 Criteria for Clinical Studies To Test
Efficacy of Products Claiming To Control Plaque
Formation To Support Their Acceptance by the
American Dental Association4
●
Characteristics of the study population should
represent those of typical product users.
●
Active products should be used in a normal regimen
and compared with placebo control or, where
applicable, an active control.
●
Crossover or parallel design studies are acceptable.
●
Studies should last a minimum of 6 months.
●
Two studies conducted by independent investigators
are required.
●
Microbiologic sampling should estimate plaque
qualitatively to complement indexes that measure
plaque quantitatively.
●
Plaque and gingivitis scoring and microbiologic
sampling should be conducted at baseline, at 6
months, and at an intermediate period.
●
Microbiologic profile should demonstrate that
pathogenic or opportunistic microorganisms do not
develop over the course of the study.
●
The toxicologic profile of products should include
the results of carcinogenicity and mutagenicity
assays in addition to generally recognized tests for
drug safety.
and over-the-counter oral hygiene products.
These testing guidelines do not, however, apply
to those toothpastes marketed as “anticalculus”
products, because the ADA considers the action
of these toothpastes in inhibiting the re-forma-
tion of supragingival calculus after a prophylac-
tic treatment (discussed later) to be cosmetic
rather than therapeutic.
Day-to-day plaque control in the healthy
individual must be separated from the use of
antibiotics or other medications in the treat-
ment of established disease. Antibiotics have no
place in prophylactic control.
Chlorhexidine
Chlorhexidine gluconate (CHX) has been used
effectively in the form of a mouthrinse (10 ml
0.2%, once or twice daily), a topical gel applied
by dental professionals (1.0% to 2.0% daily), a
toothpaste (0.4% to 1.0%), a chewing gum with
xylitol,108 a spray,34 and a direct injection into
periodontal pockets. When introduced into the
oral cavity, CHX adheres to anionic substrates
and is released over 8-12 hours. Mucosal and
gingival penetration is minimal, and it is poorly
absorbed from the gastrointestinal tract.46 CHX
has a wide range of bactericidal action, and its
selective effect against Streptococcus mutans
makes it of value in caries control in patients
with special problems.28,124,125
Early short-term studies found that CHX
rinses inhibited the formation of plaque almost
completely.81,82 However, because these initial
studies were conducted with periodontally
healthy dental students who ceased routine oral
hygiene procedures for the study duration, the
generalizability of these findings is doubtful.
Results of short-term studies by other researchers
using CHX in gels and toothpastes were less
clear-cut and revealed some undesirable side
effects.19,38 Staining of teeth and restorations, for
example, was a persistent problem.
Results of longer-term studies, conducted
over 2 years, showed that the routine use of
CHX was not appropriate. One study found
no changes in plaque and gingivitis levels
among the dental students who were the test
subjects, although again their initial excellent
oral hygiene status could have masked any ben-
eficial effects of the CHX.59 Another found
reduced levels of plaque and gingivitis in a
2-year study (also involving dental and medical
students), although one perplexing finding
was that supragingival calculus deposition
increased in the test group.83 Other 6-month
studies have also reported increased deposition
of supragingival calculus,50,67 although in
both studies it was considered of no clinical
consequence.
By the end of the 1970s, the limitations in
the routine use of CHX were widely accepted,
although it was clear that CHX could play a use-
ful role in plaque control. The side effect of
staining, plus the chance that resistant organ-
isms could develop, were enough to produce
warnings from leading periodontists against the
indiscriminate use of CHX.80 In addition, CHX
does not affect subgingival plaque, which
means that its preventive effect in periodontal
diseases is limited to preventing the deposition
of supragingival plaque after a professional
cleansing. Subsequent research has confirmed
these earlier findings. European and American

studies of 6 months’ duration confirmed that
use of CHX, whether as a twice-daily rinse with
a 0.12% formulation or applied in other forms
and concentrations, reduced gingivitis, gingival
bleeding, and plaque deposits.2,12,50,67
CHX has been used for years in much of
Europe as an antiseptic rinse before oral sur-
gery, to improve plaque control up to 3-4 weeks
after periodontal surgery, and as an oral
hygiene aid for patients with immobilized jaws
recovering from fractures. This limited and
selective application of CHX, because of its
well-documented undesirable side effects, is
also its recommended role in the United States
and Canada.
CHX is marketed in the United States under
the brand name of Peridex. It has been accepted
by the ADA6 as a safe and effective antiplaque
agent under the 1986 ADA guidelines (see Box
29-2). Its use should be restricted to patients
with periodontitis, and it has no public health
applications.
Other Antibacterial Compounds
In short-term studies, alexidine dihydrochloride
mouthrinse (10-15 ml, 0.035%-0.05%) has
yielded results similar to those found for CHX.
Reductions in plaque and gingivitis were
recorded,36,77,119 although some reductions
were of little clinical importance.29,109 Mild
staining was also reported in all of these studies.
Mouthrinses using octenidine94 and cetylpyri-
dinium chloride9 have been tested with mixed
results; sanguinarine has been tested with
some reported success.47,63,116 The over-the-
counter mouthrinse Listerine, in which essential
oils are the active ingredients, as been accepted
by the ADA as a safe and effective antiplaque
rinse5 under its 1986 guidelines. Mouthrinses
combining CHX and essential oils are also
effective.104
Stannous fluoride also seems to have anti-
plaque properties, probably because it affects
the growth and adherence of bacteria rather
than because it exerts a direct bactericidal
action. Stabilization of stannous fluoride in an
anhydrous formulation, instead of in an aque-
ous preparation, has increased its efficacy.91
Stabilized stannous fluoride at 0.454% in a
toothpaste reduces gingivitis, although this
product was found to be no better than a
control toothpaste (with sodium fluoride only)
29 Prevention of Periodontal Diseases 401
in restricting the buildup of supragingival
plaque.20,95
Toothpastes with baking soda and peroxide
(together) are marketed as plaque inhibitors,
but clinical trials and in vivo testing have pro-
vided no evidence for efficacy in reducing
plaque buildup and gingivitis following a pro-
phylactic treatment.15,21,114 The performance of
a baking soda and peroxide toothpaste was
notably inferior to that of a stabilized stannous
fluoride product in the same test.21
Anticalculus (“Tartar-Control”)
Toothpastes
Efforts to find a toothpaste ingredient that pre-
vents the formation of calculus on teeth go back
a long way,57,112 and until recently they were
not successful. However, research during the
1960s found that pyrophosphate prevented cal-
cification by interfering with the conversion of
amorphous calcium phosphate to hydroxy-
apatite.41 When this was added to the finding
that the concentration of pyrophosphate in the
plaque of low calculus formers was higher than
in the plaque of high calculus formers,37 the
stage was set for testing the anticalculus effect of
pyrophosphate in toothpaste.86 Commercially
marketed anticalculus toothpastes mostly con-
tain a mix of soluble pyrophosphates at 3.3%
concentration, with or without additional
ingredients. These compounds are not part of
the abrasive system of the toothpaste, and they
are independent of the fluoride added for caries
control.
A number of studies have demonstrated that
pyrophosphates can effectively inhibit the
formation of supragingival calculus after it
has been removed by a prophylactic proce-
dure.26,31,75,76,79,121 These studies were all of
fairly similar design. They ran for 2-6 months in
groups of adult subjects, mostly selected for
their propensity to form calculus quickly. All
subjects received a thorough prophylactic treat-
ment to remove all calculus and were then ran-
domly allocated to test and control groups. In
all of the studies, test subjects exposed to the
pyrophosphates were found to have consider-
ably less supragingival calculus formation than
was seen in the control subjects.
Triclosan is an antibacterial agent that
inhibits plaque buildup by adsorbing to the
tooth surface and perhaps by exerting direct
402 Prevention of Oral Diseases in Public Health
antiinflammatory effects on mediators of gingi-
val inflammation.45 It has been shown to be
highly effective at preventing plaque deposition
after a professional prophylactic treatment and
reducing gingival bleeding, especially when it is
combined with a copolymer of methoxyethyl-
ene and maleic acid.44 Studies have shown the
efficacy of triclosan (compared to a toothpaste
with only sodium fluoride as an active ingredi-
ent) when used as a mouthrinse at 0.1% or
0.2%,58 or at 0.3% concentration in a tooth-
paste with 2% copolymer.25,60,93,98 Efficacy of
the triclosan-copolymer formulation is inde-
pendent of the type of fluoride used in the
toothpaste, and it is more effective than a fluo-
ride-only dentifrice at reducing existing plaque
and gingivitis.72 Studies of triclosan-copolymer
and other ingredients such as pyrophosphates
and zinc citrate have given generally positive
results,18,35,39,51,105 and work on these formula-
tions is continuing.
What these anticalculus toothpastes do and
do not do must be noted. They inhibit the dep-
osition of new supragingival calculus after a
professional cleaning, and do so without
adverse tissue reaction. Triclosan-copolymer
has been shown to reduce existing plaque and
gingivitis.72 These toothpastes do not remove
existing supragingival calculus, and they have
no effect on existing subgingival calculus. The
ADA’s website lists a number of toothpastes that
have been accepted as being tartar-control as
well as anticavity products, and the number is
likely to continue growing.
The marketing of constantly more effective
plaque-control toothpastes that otherwise do
not affect the oral ecology can only lead to fur-
ther improvements in oral hygiene and reduc-
tion in gingivitis. It is reasonable to assume that
adult periodontitis should also be reduced in
time, although there is no evidence yet to show
that this happens. We also do not yet know if
these products have any impact on aggressive
periodontitis, although because of the compro-
mised host etiology of that condition they are
likely to be less effective in such cases.
COMMUNITY-BASED CONTROL
OF PERIODONTAL DISEASES
Until some means can be found to enhance the
host response of susceptible persons, there will
always be a minority of individuals who are at
special risk of losing teeth from periodontitis.
Oral hygiene is especially important in such
individuals, even though periodontal infections
may represent only part of the disease problem
(compromised host response is the rest of it and
is little affected by oral hygiene).
Public programs of dental health education
aimed at improving general standards of oral
hygiene have long been a mainstay of dental
public health. Their effectiveness is hard to
demonstrate, even though it is likely that public
standards of oral hygiene are continuing to
improve. Because oral hygiene is of high cul-
tural value, extensive and sophisticated com-
mercial advertising must have made a strong
impact on public oral hygiene behavior. As a
result, the potential additional impact of organ-
ized programs of oral hygiene education need
to be carefully thought through before such
programs are launched. They are likely to be of
most value when directed at populations that
have little exposure to commercial advertising
or that do not espouse the middle-class values
of oral hygiene assumed by media advertising.
Public education in oral hygiene is useful in
many developing countries, although the pro-
grams should always be monitored periodically
for effectiveness.
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 30 Restricting the Use of Tobacco
PREVALENCE OF TOBACCO USE
PATHOLOGIC EFFECTS OF SMOKELESS
TOBACCO
RESTRICTING TOBACCO USE
Tobacco use is a major risk factor for many dis-
eases, and it is the leading cause of preventable
mortality.34 The bare statistics are brutal: more
than 430,000 deaths occur each year attributa-
ble to tobacco use in the United States, and
some 3000 children and adolescents become
new smokers every day. More than 10 million
Americans lost their lives prematurely to
tobacco-caused diseases during the twentieth
century.54 The annual global death toll was over
4 million in 1998, and at current rates will
exceed 8 million by 2020.62 There is some hope
that tobacco control measures will be having an
effect by then, because in 2003 the World
Health Organization (WHO) concluded a
remarkable worldwide Framework Convention
on Tobacco Control. This convention calls for
health promotional activities among member
nations to control tobacco use by a variety of
methods.63
Controlling exposure to tobacco is a public
health issue that involves all health profession-
als. Dentists and hygienists stand together with
their medical colleagues to do what they can to
reduce exposure to tobacco, including engaging
in health promotional activities on the political
front and counseling patients one to one. With
regard to oral effects, tobacco use of all kinds is
a major risk factor for oral cancer (see Chapter
23), and the degree of risk is proportional to the
extent of use. It is also a major risk factor for
periodontitis (see Chapter 21), so much so that
it may have been a major reason for high levels
of periodontitis throughout much of the twenti-
eth century.30 Estimates are that tobacco use is
Restricting Cigarette Smoking
Restricting Smokeless Tobacco
Use
WHAT DENTAL PROFESSIONALS CAN DO
responsible for half of the periodontitis and
three quarters of the oral cancer seen in the
United States.58 Even dental caries in children
has been associated with exposure to second-
hand smoke.4
Political action to reduce exposure to
tobacco is not easy because the tobacco industry
is a formidable opponent. Likewise, inducing
patients to change established tobacco habits is
difficult because tobacco addictions are power-
ful and there are usually strong social or psycho-
logical reasons why a tobacco habit was
adopted in the first place. However, as described
here, programs are in place that can help.
In this chapter, we do not detail the patho-
logic effects of cigarette smoking because this
information is readily available elsewhere. For
example, the most recent of four reports on the
health consequences of tobacco from the
Surgeon General of the United States describes
the ills that come with tobacco use in remorse-
less detail (http://www.surgeongeneral.gov/
library/smokingconsequences). However, we
do review the evidence for the pathologic effects
of smokeless tobacco, because these have not
received the same degree of research attention.
This chapter describes the prevalence of smok-
ing and smokeless tobacco use and then looks
at the various initiatives that aim to reduce
exposure to tobacco in all its forms. These
include the programs that dental professionals
can use in their practices to help patients quit.
Attention is also given to the specific public
health issue of reducing the use of smokeless
tobacco among young people. The abbreviation
407
408 Prevention of Oral Diseases in Public Health
ST is used for smokeless tobacco products; read-
ers can take it as standing for either “smokeless
tobacco” or “spit tobacco,” according to taste.
PREVALENCE OF TOBACCO USE
Prevalence of cigarette smoking in the United
States is now around 23% among adults and has
remained around that figure for some years.52
Smoking prevalence has been cut in half since
the first Surgeon General’s report on smoking
and health in 1964, and this progress is rightly
considered one of the 10 greatest public health
achievements of the twentieth century.56 The
sobering aspect of this achievement is that most
of those who intend to quit have probably
already done so, and those who are left are the
hard-core smokers, plus the 3000 new young
people who start smoking each day. (It is a fair
bet that few current smokers in the United States
have even heard of WHO’s framework conven-
tion.) Data on smoking in the United States are
presented in Box 30-1. The report is mixed, with
the main concerns now centered on youth
smoking and the concentration of tobacco use
in lower socioeconomic groups.
Heavy marketing of ST products, principally
targeted to adolescent and young adult males,
has coincided with the national decline in ciga-
rette smoking. Marketing of ST seems to have
been successful; consumption of ST products in
the United States almost tripled between 1972
and 1991.49 It was estimated from a national
survey that, in 1991, 5.3 million American
adults (2.9% of the population) were using ST:
4.8 million men and 533,000 women.49 This
percentage had risen slightly to 3.2% of the
population by 1999.53
The concerns about ST’s appeal to youth
seem well founded: 1995 national survey data
revealed that 11.4% of high school students had
used ST within the previous 30 days, 19.7% of
males and 2.4% of females. ST use among
whites was 14.5%, among African-Americans
2.2%, and among Hispanic students 4.4%.31
The 1991 national survey found that 8.2% of
males ages 18-24 years were regular ST users, the
highest proportion of any age-group. Even if
there is some overreporting,15 presumably by
individuals who wish to appear more “macho,”
these figures are high. Among adults 45 years of
age or older, however, ST use was more com-
mon among African-Americans than among
whites.21 Usage of ST is highest in the South, in
rural areas, and declines with increasing educa-
tion.49 Women users of ST are predominantly in
the South.59
Use of ST is extensive in the military8,26 and is
particularly heavy among Native Americans; a
study conducted in seven western states found
that 56% of Native Americans in the ninth and
tenth grades reported that they were regular
users,11 as were 28.1% of sixth-graders.7 ST use
among Native American women is substantially
above the national rate for women.44 Native
Americans emerge as the ethnic group with the
heaviest relative use of ST and the only one in
which there is almost equivalent use among
males and females.11,61 In one study of Navajo
adolescents, over 25% of ST users were found to
have leukoplakia, compared to only 4% of
nonusers. The duration and frequency of use were
highly significant risk factors for leukoplakia.61
Prevalence of ST use is also widespread
among highly visible professional baseball
players; surveys carried out with major and
minor league teams found that 39%-46% of
players were regular users.19,60 Another study of
baseball players in 1988 found that ST users
had 60 times the risk of developing leukoplakia
compared with nonusers.25
The remarkably high occurrence of oral can-
cer in India (see Chapter 23) is thought to result
from the high prevalence of tobacco chewing in
several forms. Because the rate of conversion of
leukoplakia and other precancerous lesions to
oral cancer is no higher in India than else-
where,45 it seems to be the high exposure to
tobacco, rather than any inherent characteristics
of Indian people, that leads to the high preva-
lence of leukoplakia, and subsequently oral
cancer, in that country.
Since the pathologic effects of cigarette
smoking are now extensively documented,
tobacco marketing aims to foster the perception
that ST is a less risky substitute for cigarettes.
However, ST is far from harmless.
PATHOLOGIC EFFECTS
OF SMOKELESS TOBACCO
ST is a particularly worrisome form of tobacco,
because its current use by young people
has the potential to increase the incidence of

BOX 30-1 Facts on Smoking Prevalence in the United States, 200154
●
In 2001, 46.2 million adults (22.8%) in the United
States were current smokers: 25.2% of men and
20.7% of women.
●
Among racial and ethnic groups, smoking prevalence
was highest among American Indians and Alaskan
natives (32.7%) and lowest among Hispanics (16.7%)
and Asians (12.4%).
●
Among income groups, smoking prevalence was
higher among adults living below the poverty level
(31.4%) than among those at or above the poverty
level (23%).
●
Smoking prevalence was highest among those ages
18-24 (26.9%) and 25-44 (25.8%) and lowest among
those age 65 and older (10.1%).
●
Among current adult smokers, 37.8 million (81.8%)
smoked every day, and 8.4 million (18.2%) smoked
some days.
●
An estimated 44.7 million adults were former
smokers in 2001, representing 49.2% of all those
who had ever smoked. An estimated 15.3 million
adult smokers had stopped smoking for at least 1 day
during the preceding 12 months because they were
trying to quit.
●
Adults who had earned a General Educational
Development (GED) diploma (47.8%) and those with a
grade 9-11 education (34.3%) showed the highest
prevalence of smoking; those with master’s,
professional, and doctoral degrees showed the lowest
prevalence (9.5%).
●
Smoking prevalence data for combined years 1965-66
through 2000-01 indicate a slow but steady decrease
among both African-Americans and whites.
oral cancer in the future. 40 The American
Dental Association (ADA) has firmly stated
policies opposing any use of ST, and the ADA
clearly rejects ST as a substitute for regular
tobacco.5
ST is sold in several forms. The main concern
is with snuff, a powdered tobacco product,
which is used by placing a “dip” between the
cheek and gum. Dry snuff contains high con-
centrations of N-nitrosamines2,27; evidence is
strong that compounds in this group are
carcinogens, especially for oral cancers.27,39
The N-nitroso compounds found in snuff are
DNA-damaging agents in cancers of the aerodi-
30 Restricting the Use of Tobacco 409
●
In 2000-01, for the first time, smoking prevalence
among African-American men was similar to that
among white men. Since 1970-74, prevalence has
declined more rapidly among African-American men
than among white men.
●
In 2000-01, smoking prevalence also declined more
rapidly among African-American women than
among white women. Prevalence among African-
American women has been generally lower than
among white women since 1993-95. Before 1993-
95, prevalence of current smoking generally was
comparable among African-American and white
women.
●
The overall decline in cigarette smoking prevalence
in the adult U.S. population is not occurring at a rate
that will meet the national health objective for 2010
of 12%.
●
In 2000, the Surgeon General concluded that the 2010
objective could be attained only if comprehensive
approaches to tobacco control were implemented.
Sustained or increasing implementation of
comprehensive tobacco-control programs to meet the
funding levels recommended by the Centers for
Disease Control and Prevention are necessary to
attain the 2010 national objective.
●
Comprehensive programs that focus on reducing
tobacco use among those in different socioeconomic
strata, those in different racial and ethnic populations,
and groups with different educational levels could
help reduce cigarette smoking and tobacco use in
general and reduce the extensive morbidity, mortality,
and economic costs associated with tobacco use.
gestive tract.35 A consensus panel of the
National Institutes of Health found strong evi-
dence that use of snuff causes oral cancers,38 a
conclusion for which there was ample support
at the time47,57 and subsequently.3,17,27,29
Nicotine is absorbed from ST in amounts simi-
lar to those absorbed from cigarette smoke,9
which makes ST a potential risk factor for the
same diseases that result from smoking. That
could be why ST users face a relative risk of 2.1
for cardiovascular disease compared to
nonusers. The relative risk for smokers com-
pared to nonsmokers in the same study was
3.2.10
410 Prevention of Oral Diseases in Public Health
The continued use of snuff leads to localized
tissue changes, most commonly the develop-
ment of leukoplakia, which is characterized by
the appearance of white, wrinkled mucosa at
the site where the snuff is placed. Leukoplakia
can become cancerous in 3%-5% of cases,45
although there is also evidence that these
lesions can be reversed if the ST habit is
ended.22,33 With regard to oral conditions other
than precancerous soft tissue changes, no good
evidence exists that ST can cause caries and peri-
odontal diseases. Gingival recession at the site
where the quid or dip is placed is common,
however. It has also been found that poor oral
hygiene among ST users contributes to the for-
mation of nitrosamines in the oral cavity.35
Further evidence for the carcinogenic poten-
tial of chewing tobacco comes from studies of
women smokers and dippers in the South59
which found that the relative risk of developing
cancer of the gums and buccal mucosa was 4.6
for smokers (i.e., smokers developed oral cancer
at 4.6 times the frequency of nonsmokers).
However, for users of ST the relative risk was 13-
48, with higher risk found in those with longer
ST use.
RESTRICTING TOBACCO USE
Restricting Cigarette Smoking
There are good reasons why the early twenty-
first century is a good time for a national
campaign for smoking cessation (Box 30-2).
Funding for such a program looked promising
in 1998, when the Master Settlement Agree-
BOX 30-2 Reasons Why the Early Twenty-First Century Is an Ideal Time for Bold Steps To Reduce Tobacco
Use in the United States20
●
Although health care funding is scarce, tobacco-
related diseases cost $150 billion each year.
●
Although numerous effective tobacco-dependence
treatments exist, millions of tobacco users are unable
to obtain or afford such treatments.
●
A major funding source, the 1998 Master Settlement
Agreement between the states and the tobacco
companies, is being used to plug states’ budgetary
ment with the tobacco companies seemed to
ensure seemingly infinite funding to the states
for cessation programs.24 At a time when court
actions against the tobacco industry were accu-
mulating, the Master Settlement Agreement was
negotiated between the tobacco industry, on the
one hand, and a group of state attorneys gen-
eral, private lawyers, and public health advo-
cates on the other. Under the terms of the
settlement, the tobacco industry would get
relief from present and future litigation pay-
ments, and in exchange would accept some
additional regulation of advertising and would
make substantial cash payments to state govern-
ments. These payments were intended to be
used for tobacco control programs, although
few states have used these funds for that pur-
pose—because of many states’ budgetary prob-
lems soon after the settlement, the funds were
diverted to become a general-purpose emer-
gency revenue stream.23 Among other funding
problems, in only 36 states do Medicaid pro-
grams pay for smoking cessation treatment,
including pharmacotherapy, nicotine nasal
sprays, nicotine inhalers, nicotine patches, and
nicotine gum.28 This is despite the fact that a
higher proportion of Medicaid recipients
smoke than do members of the general
population.42
Despite these stumbling blocks, progress
continues to be made on tobacco control.
Smoke-free indoor air, especially in bars and
restaurants, has been mandated in many local
communities and even at the state level in six
cases (California, Connecticut, Delaware,
shortfalls rather than to promote smoking
cessation.
●
Although the devastating impact of tobacco use on
health has been exhaustively documented, the
tobacco industry continues to lure adolescents and
adults into tobacco dependence through an $11
billion advertising and promotional effort.

Florida, Maine, and New York). Although the
Master Settlement Agreement is not working as
its backers intended, the public discussions it
sparked have served to increase public knowl-
edge and awareness.
The research attention devoted to smoking
has lead to development of some effective inter-
ventions.50 These have been put into program
plans, intended for both private practice and
public health applications, that are built on the
tobacco-related objectives of Healthy People 2010
(see Chapter 5). One plan for community
interventions came from the Task Force on
Community Preventive Services, an independ-
ent (though Centers for Disease Control and
Prevention–supported) group of health experts
that is developing a guide to community serv-
ices on a variety of health issues. The task force
goals were to direct interventions toward
(1) reducing overall exposure to environmental
tobacco smoke, (2) reducing tobacco use initia-
tion, and (3) increasing the cessation of tobacco
use.48 The Task Force has conducted a series of
systematic reviews to identify the most effective
interventions, and its work is continuing.
Strongly recommended interventions to date
include establishment of smoking bans and
restrictions, increase in the unit price for
tobacco products, and mass media education.48
Restricting Smokeless Tobacco Use
Preventive efforts against the diseases that come
with ST use are based principally on public and
individual education to convince people to
BOX 30-3 Major Provisions of Public Law 99-252, the Comprehensive Smokeless Tobacco Health Education
Act (February 1986)32
●
Development and implementation of health education
programs and materials to inform the public of health
risks resulting from the use of smokeless tobacco
products.
●
Inclusion of health warning labels on all smokeless
tobacco products and advertisements, except those
on outdoor billboards.
●
Prohibition of radio and television advertising,
beginning in August 1986.
30 Restricting the Use of Tobacco 411
drop the habit or, preferably, not to begin in the
first place. The public health efforts of the
various professions involved received a boost
with the passage of Public Law 99-252, the
Comprehensive Smokeless Tobacco Health
Education Act, in February 1986. The most rele-
vant details of this legislation are shown in
Box 30-3.
Ironically, this national legislation was sup-
ported by the tobacco industry, which was
spurred to do so because of the likelihood that a
majority of states would pass more severe laws
of their own.13 The growth of public concern
about the marketing of ST was stimulated by the
publicity generated by the 1985 case of Marsee v
US Tobacco Company. Sean Marsee, a top high
school athlete, died of oral cancer at age 19 after
years of ST use. The suit was brought by Sean’s
mother, who charged that the tobacco company
engaged in misleading advertising and failed to
place warnings on its products.13 Although Ms.
Marsee’s suit was not successful, the case engen-
dered a great deal of sympathy and concern.
Voluntarily breaking the ST habit, given that
nicotine addiction is involved, seems to be no
easier than breaking the cigarette habit. Of 25
adolescent habitual ST users who participated
in an intensive program of ST cessation, only
4 had remained successful in quitting 3 months
after the program.18 On the other hand, in
another intervention study the number of
young male ST users who quit was 50% above
the normal rate when participants viewed a
9-minute videotape, were given a self-help
●
Disclosure to the Secretary of Health and Human
Services of the ingredients used in the production of
smokeless tobacco as well as the quantity of nicotine
in such products.
●
Technical assistance in public health education for the
states.
●
Authorization of research on the effects of smokeless
tobacco.
412 Prevention of Oral Diseases in Public Health
manual, and received an explanation of the
risks and “unequivocal advice” to quit.46
With this mixed evidence on quitting, strat-
egy should be aimed at preventing young peo-
ple from starting to use ST, although it is
obvious that health education programs need
to go well beyond the admonition to “just say
no” if they are to be successful. In the 1991
national survey, 22.9% of current ST users
reported that they currently smoked, and
another 33.3% had formerly smoked.49 Many
ST users report using ST concurrently with alco-
hol, cigarettes, and marijuana, and peer pres-
sure is a strong influence in getting started.6 The
relationship between cigarette smoking and ST
use, as well as other correlates of the habit, is
complex and needs further study if education to
discourage commencement of either habit is to
be successful.43 Ignorance of the health conse-
quences is common. A Pennsylvania study
reported that nearly half the males in grades 7-
12 did not believe that ST was harmful.14 As in
any health education for adolescents, the
immediately negative effects of ST use (stained
teeth, bad breath) can make a greater impres-
sion than the long-term health hazards.16
Multifaceted strategies were needed to imple-
ment the provisions of Public Law 99-252 (see
Box 30-3), and a leading role was played by
state and local public health agencies.12 Some
states established programs of media advertis-
ing and school health education aimed specifi-
cally at discouraging the start of ST use.
Monitoring the impact of these educational
efforts requires considerable survey effort. The
monitoring process is proceeding through a
series of institutionalized surveys,21,31 but
progress toward reducing ST use is slow. Trends
in ST use in Indiana, Iowa, Montana, and West
Virginia between 1988 and 1993 showed little
change over that period, a finding attributed to
increased advertising and promotion by the
tobacco industry, despite the existence of Public
Law 99-252.37 Minors still seem to have rela-
tively little trouble obtaining ST, even in states
where such sales are prohibited by law.1
WHAT DENTAL PROFESSIONALS
CAN DO
Dental professionals obviously have a poten-
tially major role to play in educating patients
about the hazards of ST use and in helping
patients who are already addicted to quit. The
task sounds daunting, but it can be done. The
National Cancer Institute, one of the National
Institutes of Health, funds the National Dental
Tobacco-Free Steering Committee, a broadly
based group whose mission is to promote
tobacco use cessation activities through the
dental office. Oral Health America sponsors
the National Spit Tobacco Education Program
(NSTEP; http://www.nstep.org/nstep.shtml),
funded largely by the Robert Wood Johnson
Foundation, a group that achieved national
prominence largely through its charismatic,
highly visible national honorary chairman,
baseball legend Joe Garagiola. Mr. Garagiola
hammers the message that ST use is not a tradi-
tional part of the great American pastime, no
matter how the tobacco companies try to make
it appear so.
For practitioners helping a patient to quit
smoking, there is the clinical practice guideline
Treating Tobacco Use and Dependence sponsored
by the U.S. Public Health Service in collabora-
tion with an array of governmental agencies,
educational associations, and practitioner
groups.51 The initial recommendations of this
group are shown in Box 30-4, and the website
provides a highly detailed approach to working
with patients in their attempts to quit
(http://www.surgeongeneral.gov/tobacco/clin-
pack.html). The clinical practice guideline is
interactive and constantly being updated as new
research is completed. The National Cancer
Institute has a special website devoted entirely
to providing a wealth of how-to-quit informa-
tion that both health professionals and patients
can use.36 An abundance of information on
interventions at both the individual and
community levels can also be found in The Guide
to Community Preventive Services.55 The ADA, with
assistance from some grant funding, has also
committed a lot of resources to training dentists
in tobacco use cessation techniques. When pro-
tocols are finalized, these training sessions
should become readily available to all dentists.
Use of these sources of information should
be part of the routines of every dental office, for
tobacco use cessation must be seen as the first
treatment priority for almost any oral disease.
After all, tobacco use is a serious matter—in
fact, it is a matter of life and death.

BOX 30-4 Conclusions and Recommendations on Ways Health Professionals Can Help Patients Stop
Smoking51
1. Tobacco dependence is a chronic condition that often
requires repeated intervention. However, effective
treatments exist that can produce long-term or even
permanent abstinence.
2. Because effective tobacco dependence treatments
are available, every patient who uses tobacco should
be offered at least one of these treatments:
a. Patients willing to try to quit tobacco use should
be provided with treatments identified as effective
in this guideline.
b. Patients unwilling to try to quit tobacco use
should be provided with a brief intervention
designed to increase their motivation to quit.
3. It is essential that clinicians and health care delivery
systems (including administrators, insurers, and
purchasers) institutionalize the consistent
identification, documentation, and treatment of every
tobacco user seen in a health care setting.
4. Brief tobacco dependence treatment is effective, and
every patient who uses tobacco should be offered at
least brief treatment.
5. There is a strong dose-response relation between the
intensity of tobacco dependence counseling and its
effectiveness. Treatments involving person-to-
person contact (via individual, group, or proactive
telephone counseling) are consistently effective, and
their effectiveness increases with treatment intensity
(e.g., minutes of contact).
6. Three types of counseling and behavioral therapies
have been found to be especially effective and should
be used with all patients attempting tobacco
cessation:
a. Provision of practical counseling (problem-
solving and skills training);
b. Provision of social support as part of treatment
(intratreatment social support); and
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38. NIH Consensus Development Panel. National
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39. Preston-Martin S, Correa P. Epidemiological evidence
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40. Projected smoking-related deaths among youth—
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41. Rodu B. An alternative approach to smoking control
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42. Schauffler HH, Mordavsky J, Barker D, Orleans CT.
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43. Severson HH. Psychosocial factors in the use of smoke-
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45. Squier CA. Smokeless tobacco and oral cancer: A cause
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46. Stevens VJ, Severson H, Lichtenstein E, et al. Making the
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47. Stockwell HG, Lyman GH. Impact of smoking and
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48. Task Force on Community Preventive Services.
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49. Use of smokeless tobacco among adults—United States
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50. US Public Health Service. Treating tobacco use
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51. US Public Health Service. Clinician’s packet: Treating
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52. US Public Health Service, Centers for Disease Control
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53. US Public Health Service, Centers for Disease Control
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55. US Public Health Service, Centers for Disease Control
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56. US Public Health Service, Centers for Disease Control
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A American Dental Association (ADA)
Access, patient. See Dental care, access
problems in.
Acidogenicity
of apple, 386
of sugars, 381b, 387, 388f
Acquired immunodeficiency
syndrome. See AIDS (acquired
immunodeficiency syndrome).
ADA. See American Dental
Association (ADA).
ADHA (American Dental Hygienists
Association). See American
Dental Hygienists Association
(ADHA).
Advertising, journals with, 156
African-Americans. See also Race.
life-expectancy of, 14
NDA founded by, 8
population demographics for, 14,
17, 17f
Age
baby-boomer distribution by, 15,
15f, 16f
caries distribution related to, 239-
241, 240f, 250-251, 250f, 251f
dental care utilization related to,
19-20, 20f, 21f, 23f, 130-132
oral cancer related to, 295, 295f-297f
periodontal disease and, 264f-268f,
268-269
population distribution by, 15, 15f,
16f, 130-132, 131f, 132f
root caries distribution by, 250-251,
250f, 251f
tooth loss by, 224f, 227f-229f
AIDS (acquired immunodeficiency
syndrome)
dentists with, 142-143
drug treatment for, 141
ethics standards for care in, 28-29
global extent of, 141-142, 141b
oral manifestations of, 142-143
T lymphocytes in, 140-141
timeline of, 141
transmission of, 141-142
Alcohols, “sugar,” 382, 385-386
Alexidine dihydrochloride, 401
Amalgam restorations
ADA recommendations related to,
147-149
mercury leakage from, 147-149
American Dental Association (ADA),
7-8
AIDS-related code of ethics of, 28-29
amalgam mercury
recommendations of, 28-29
416
INDEX
(Continued)
antiplaque agent guidelines of, 399-
402, 400b
dental auxillaries opposed by, 122
dentistry role of, 7-8, 7b
founding of, 7-8
public image promoted by, 8
structure of, 7-8
American Dental Hygienists
Association (ADHA), 9-10
AIDS in code of ethics of, 29
founding of, 9-10
American Society of Dental
Surgeons, 4
Amylase, 381b
Anthropology, caries studies in, 248
Apple
acidogenicity of, 386
plaque not removed by, 386
Areca nut, 298
Asians. See also Race.
population demographics of, 17,
17f
Aspartame, 385
Association of State and Territorial
Dental Directors (ASTDD), 40
Attachment loss. See CAL (clinical
attachment loss).
Australia, population growth rate in,
16f
Auxillaries. See Dental auxillaries.
B Fluoridation.
Baby-boomers
age distribution of, 15, 15f, 16f
population demographics of, 14-
15, 15f, 16f
Bacteria
caries prediction role of, 46, 245
fluoride inhibition of, 319, 319b,
401
periodontitis role of, 272
plaque associated with, 394-395,
400-401
risk factor role of, 245
Bandura’s social learning theory, 52
Belmont Report, 32
Betel nut, 298
Biomedical databases, 160-161
bis-GMA formulation, 366-367
Black, G.V., 4
Bleeding, gingival, 203-204, 204b
Blood, standard precautions related
to, 138-140
Bloodborne pathogen precautions,
139-140
Blue Cross and Blue Shield, 93
Bodily fluids. See Infection control;
Standard precautions.
Bone mineral density, fluoride not
affecting, 316-317
BOP (bleeding on probing), 203,
204b
Bradford Hill criteria, 173-174, 174b
Brushes. See Toothbrushes.
Burst theory, 262
C
CAL (clinical attachment loss), 204-
205, 204b
periodontal disease and, 204-205,
205f, 206b, 263-266, 264f,
265f
Calculus, 394-395
anticalculus toothpaste effect on,
401-402
epidemiology of, 207, 207b
measurement and diagnosis of, 207,
207b
Candidiasis, oral, AIDS/HIV with, 142
Capitalism, 27
Capitation reimbursement plan, 89-90
Carbohydrates, 233-252. See also
Starches; Sugars.
caries role of, 245-250
fermentable, 381b
Cardiovascular disorders,
periodontitis with, 276-277
Caries, 194-200, 233-252. See also
age group with, 239-241, 240f, 250f
bacterial strains and
predictions related to, 46
risk factor role of, 245
cavitation in, 197b
coronal, 196-198, 197b
diet role in, 245-250, 380-389
distribution of
by country, 233-236, 234t, 235f,
235t
children and, 233-245, 236f-
238f, 240f, 242f
global, 233-236, 234t, 235f, 235t
regional U.S., 238-239, 240f
secular variations in, 236-237,
236f
socioeconomic status in, 243-
245, 244f
uneven, 237-238, 238b, 238f-
240f
early childhood, 199, 199t, 252
epidemiologic aspects of, 194-200,
195b, 197b, 198b, 199t

Caries (Continued)
examination of tooth for, 196-198,
197b
genetic factors affecting, 245
hidden, 198
history of, 233
measurement and diagnosis of,
194-200
D1-D3 Scale in, 196-198, 197b
Dichotomous Scale in, 196-198,
197b
DMF Index in, 194-196, 195b
newer techniques for, 198
nutrition role in, 245-250, 380-389
race factors in, 239-241, 240f
reversibility of, 196
root, 198-199, 198b, 250-251, 250f,
251f
sugars and starches role in, 245-
250, 380-389, 381b, 383f,
384f, 388f
treatment needs assessment of, 199-
200
Causality
Bradford Hill criteria for, 173-174,
174b
research studies role of, 173-176,
174b
Cavitation, caries with, 197b
Census. See Population.
Centers for Disease Control,
fluoridation oversight by, 330-
331, 331b
CFI (Community Fluorosis Index),
210, 211f, 212f
Cheese, anticariogenicity of, 386
Chemotherapeutic oral hygiene
products, 399-402, 400b
Children
baby bottle caries affecting, 199,
199t, 252
caries distribution in, 233-245,
236f-239f, 238b, 240f
dental care financing aid for, 103-
108
fissure sealant use in, 370-375,
373t, 374f
fluoridation with caries reduction
in, 317-318, 334, 347-360,
350t, 353t, 359t
Chlorhexidine
dental products containing, 400-
401
oral hygiene use of, 400-401
Cholera epidemic, historic London in,
184, 185f
Cleft lip and palate, 299-300
epidemiologic measurement of,
216, 300
genetic factors in, 299-300
public resources for, 107
risk factors for, 299-300
Climate, fluoridation affected by, 326-
328, 327t
Clinical attachment loss (CAL), 204-
205, 204b
periodontal disease and, 204-205,
205f, 206b, 263-266, 264f,
265f
Clinical Queries database, 160
Cochrane Collaboration Database,
167-168, 167b
Code of ethics. See also Ethics.
AIDS/HIV patient and, 28-29
professionalism requirement for, 4
Commercial model, 3
Community
amenities provided by, 51-52, 51b
dentistry profession history in, 3-10
health promotion based in, 50-53,
51b
service to, ADA code for, 29-30
Community Fluorosis Index (CFI),
210, 211f, 212f
Community Periodontal Index (CPI),
206-207, 206b
Compromised host. See
Immunodeficiency.
Control groups
active vs. passive, 179
research studies use of, 178-179
Corn syrup, high fructose, 383-384,
383f, 384f
Coronal caries, 196-198, 197b
Costs
dental care (national), 83-85, 85f,
86f
fissure sealant use and, 372-375,
373t, 374f
fluoridation programs with, 331b,
338-340
health care (national), 83-85, 83f-
86f
CPI (Community Periodontal Index),
206-207, 206b
D social responsibility for, 26-28,
DAI (Dental Aesthetic Index), 217
Databases
biomedical, 160-161
Cochrane Collaboration Database
in, 167-168, 167b
journal articles in, 158-161
PubMed, 160
D1-D3 Scale caries assessment, 196-
198, 197b
DDE (Developmental Defects of
Dental Enamel Index), 213-
215, 214t
Dean, H. Trendley, 210, 308-311
Dean’s Fluorosis Index, 210, 211f, 211t,
212f
cities’ water fluoride using, 211f,
212f, 328
Index 417
Dean’s Fluorosis Index (Continued)
criteria used in, 211t
fluorosis measurement using, 210,
211f, 211t, 212f
history of, 307-311, 310f, 312f
water supply fluoride related to, 212f
def index, 194-195
Delta Dental Plans, 90-93, 92f
reimbursement mode in, 91-93, 92f
Dental Aesthetic Index (DAI), 217
Dental assistants, 111-113, 112b, 120
Dental auxillaries. See also Dental
hygienists.
ADA position on, 122
dental practice activities of, 71-72,
111-113, 112b
denturists as, 123
expanded function type of, 120-
122, 121b
fissure sealants applied by, 371
laboratory technicians as, 113, 122-
123
nurses as, 113
supervision for, 112, 112b
Dental care
access problems in, 128-136
dentist/population ratio in, 129-
136, 129f
ethics of, 33-34
reasons for, 128, 129-134, 129f,
133b, 134b
scope of, 128-134
strategies for correction of, 134-
136
costs of nationally, 83-85, 85f, 86f
ethical standards in. See Ethics.
financing of, 81-108. See also
Financing; Insurance plans.
expenditures targeted by, 84-85,
85f, 86f
legislated programs related to,
26-28, 102-108
public programs in, 83-85, 85f,
86f, 102-108, 104f, 105f
102-108
third-party payment in, 86-108
history of development of, 3-10
population demographics and, 18-
23, 19f-23f, 113t, 115t
utilization of, 18-23, 19f-23f
age in, 19-20, 20f, 21f, 23f
dentate-edentulous status in, 20,
20f
education status in, 20-21, 21f
future of, 22-23
gender in, 18-19, 19f
geographic region in, 22, 22f
insurance status in, 22, 23f
need category in, 18
race and ethnicity race in, 21-22
socioeconomic status in, 20-21, 21f
418 Index
Dental education
AIDS/HIV issues in, 146-147
career destination option in, 12
continuing, 29
debt level of graduate of, 69
dentist numerosity related to, 116-
118, 117f, 129, 129f
early dentistry in, 3-4
Gies report on, 5
National Health Service Corps in,
123-124
school founding for, 4-5
subsidies available for, 124-125
twentieth century changes in, 5-6
Dental health. See Oral health.
Dental hygiene practice
ADHA role in, 9-10, 29-30
ethical standards in. See Ethics.
history of development of, 6-7, 9-10
Dental hygienists, 118-120
career destination options for, 10-12
duties of, 110
education requirements for, 6-7
independent practice by, 119-120
number of in U.S., 118, 119t
Dental implant success rates, 168
Dental practice, 67-78. See also
Dentistry; Dentists.
ADA role in, 7-8, 7b
affluent areas attraction for, 68-69,
68f
auxiliaries’ duties in, 71-72, 111-113,
112b
debt level at start of, 69
dental unit waterline issues in, 147
hospital-based, 70-71
infection control in. See Infection
control.
personnel related to, 71-72, 111-123
primary health care worker
activities in, 71-72
private, 67-69, 69f
department store clinics in, 70
franchised, 70
group vs. solo, 69, 69f
salaried vs., 10-12
public programs history in, 71-73,
101-108
quality assurance in, 73-78, 74b
activities aimed at, 76-77
cost control role of, 77-78
evolution of, 74-75
recent issues in, 75
structure-process-outcome model
for, 73-74, 74b
terminology of, 73-74, 74b
specialty fields in, 115
Dental Practice Parameters, 31
Dental public health, 40-47. See also
Fissure sealants; Fluoridation;
Public Health.
access to care factors in, 45-46
Dental public health (Continued)
accreditation for practice of, 41
core functions and services of, 40,
41b
current issues in, 45-47
data collection and use in, 42-45,
44b, 45f
definition of, 40-42, 41b
global data for, 44
planning cycle in, 45, 45f
preventive strategies aspects of, 46-47
private care goals and, 47
surveillance process used in, 42-45,
44b
surveys used in, 43-45, 44b
targeting concept in, 46-47
Dental technicians, 113, 122-123
Dentin, caries affecting, 197, 197b
Dentistry. See also Dental care; Dental
practice.
ADA role in, 7-8
career destination options for, 10-12
education for. See Dental education.
ethics role in. See Ethics.
evidence-based, 162-170. See also
Journals, systematic reviews of.
clinician responsibilities in, 168-
169
definition of, 162-163
examples of use of, 167-168, 167b
limitations of, 169-170
literature review role in, 164-169,
167b
history of development of, 3-10
journals related to. See Journals.
patient population demographics
for, 18-23, 19f-23f, 113t, 115t
professionalism models applied to,
3-4
twentieth century growth in, 5-6
Dentists, 113-118. See also Dental
practice.
AIDS/HIV transmission by, 142
distribution of, 115-116, 115t, 118
State Practice Acts affecting, 118
female proportion of, 114
foreign-trained, 114
hepatitis transmission by, 144-145
population ratios for
dental care access problems and,
129-136, 129f
other countries, 113, 113b
states, 115-116, 115t
U.S., 113-114, 113t, 115-116, 115t,
129f
supply of, 113-118
access problems related to, 129-
136, 129f
analysis of adequacy of, 129f,
130-135, 131f, 132f
education affecting, 116-118,
117f, 129, 129f
Dentists (Continued)
legislation affecting, 118, 123-
125
projected to 2020, 129-136, 129f
shortage-trending factors
affecting, 132-134, 133b, 134b
surplus-trending factors affecting,
133b, 1334b
Dentition. See Edentulism; Primary
dentition; Teeth; Tooth loss.
Dentures, oral cancer link to, 299
Denturists, 123
Depression, temporomandibular joint
dysfunction with, 301-302
Developmental Defects of Dental
Enamel Index (DDE), 213-215,
214t
df index, 195
Diabetes mellitus, periodontitis with,
274-275
Dichotomous Scale
caries assessment using, 196-198,
197b
Diet
caries role of, 245-250, 380-389
cariogenic foods in, 381-385, 381b,
383f, 384f, 388f
“cleansing” foods in, 386-387
early studies related to, 247-250,
248b
high fructose corn syrup in, 383-
384, 383f, 384f
periodontitis role of, 273
processed foods in, 381, 381b, 384
snack foods in, 382
soft drinks in, 382-383
sugars and starches in, 245-250,
380-389, 381b, 383f, 384f,
388f
Dietary supplements
dosage levels for, 350-351, 350t
fluoride in, 289, 347-351, 350t
risk due to, 350
DMF Index, 194-196, 195b
caries assessment using, 194-196,
195b
definition of, 196
half-mouth, 194
limitations of, 195b, 196
sealant teeth in, 195b, 196, 366
DMFS index, 196
DMFT index, 194
Drinking water. See Water supply.
E
Economic status. See also
Socioeconomic status.
dental care utilization related to,
20-21, 21f
population distribution by, 17
tooth loss related to, 224, 224t,
225, 227f

Edentulism, 224-226. See also Tooth
loss.
dental care utilization related to, 20,
20f, 224, 226, 230
other countries’ percentage of, 224t,
225t
patient choice role in, 55, 55b
race and ethnic differences in, 224t,
225t, 226, 227f
states’ rates of, 224-226, 226t
U.S. rate of, 224-226, 224f, 226t,
227f
Education. See also Dental education.
dental care utilization related to,
20-21, 21f
oral health promotion role of,
57-58, 58b
Enamel. See also Caries; Fluorosis.
caries affecting, 197b
fluoride effect on, 287-288, 307-
308, 319-320
mottling of, 287-288, 307-308, 319-
320
Environmental Protection Agency,
fluoride guidelines of, 327b
Epidemics
London cholera in, 184, 185f
public health aspects of, 38-39, 40
Epidemiology, 173-218
basic concepts of, 183-192
cancer measurement for, 217. See
also Oral cancer.
caries measurement for, 194-200,
233-252. See also Caries.
cleft lip and palate measurement
for, 216, 300
definition of, 173
factors affecting, 183-186, 185f,
186-192
fluorosis measurement for, 210-215.
See also Fluorosis.
historic aspects of, 184-186, 185f
malocclusion measurement for,
216-217, 300
measurement methods in, 187-189.
See also under specific diseases.
count of cases in, 187
index in, 187-188, 188b
proportions in, 187
rates in, 187
scales in, 188-189, 188b
sensitivity and specificity in, 191,
191f
periodontal disease measurement
for, 203-208. See also
Periodontal disease;
Periodontitis.
purposes of, 186b, 191-192
research studies design for, 173-
182. See also Research studies.
Erythroplakia, oral cancer role of, 299
ESI (Extent and Severity Index), 205
Ethics, 25-34
access to care challenge in, 33-34
guideline frameworks derived from,
25-26, 26b
human subject standards in, 31-33,
32b, 33b
individual vs. societal responsibility
in, 26
physician’s oath as, 30b
professionalism role of, 25-26, 26b
puritan, 27, 40
regulatory standards based on, 26,
28-33, 30b, 32b, 33b
research role of, 31-33, 32b, 33b
Ethnicity. See Race.
Evidence-based dentistry, 162-170,
167b
Examiner, reliability attribute of, 180,
189-190, 190f
Explorer, caries diagnosis using, 197,
197b
Exposure, risk factor role of, 174b,
175, 175b
Extent and Severity Index (ESI), 205
Extractions, patient choice role in, 55,
55b
Eyewear, standard precautions using,
139
F 319b, 347-360
Fauchard, Pierre, 4
FDI World Dental Federation, 9
Fees. See Financing; Insurance plans;
Reimbursement.
Females, dentistry proportion of, 114
Fetus, fluoridation affecting, 335, 351
Financing
expenditures targeted by, 84-85,
85f, 86f
fee-for-service in, 86, 87f
for-profit plans in, 93
individual vs. societal responsibility
for, 26-28, 102-108
insurance principles related to, 81-83
managed care role in, 94-99
not-for-profit plans in, 90-93
public programs in, 102-108, 104f,
105f
dental care in, 83-85, 85f, 86f,
102-108, 104f, 105f
health care in, 83-84, 83f-84f,
101-108, 102f, 103f
history of, 71-73, 101-102
third-party payment in, 86-108
Fissure sealants, 366-376
acid etch of tooth surface for, 367-
368
applied over caries, 370, 374f
attitudes toward, 375-376
clinical trial design related to, 368
cost effectiveness of, 372-375, 373t,
374f
Index 419
Fissure sealants (Continued)
DMF Index affected by, 195b, 196,
366
efficacy of, 368-370
fluoride combined with, 361-373
history of, 366-367
longevity and retention of, 369,
374f
products for, 367-368
public health programs using, 370-
372, 371f
Floss
interdental cleaning with, 396
waxed vs. unwaxed, 396
Fluoridation, 326-342
caries reduction with, 307-312, 332-
342, 347-360
adults in, 335, 336f, 347-360
cessation patterns in, 337-338,
337f
children in, 317-318, 334, 347-
360, 350t, 353t, 359t
dietary supplements in, 289, 349-
351, 350t
early studies on, 307-312, 310f,
312t, 314-316, 332-334, 333t
gel with fluoride in, 351-354,
352t
mechanism of action of, 318-320,
milk with fluoride in, 347-349
mouthrinse fluoride in, 352t,
353t, 354-355, 359t
partial-exposure effect in, 336
poor economic status role in,
333-334, 334f
salt with fluoride in, 347-348
school drinking water in, 348-
351, 350t
toothpaste fluoride in, 289, 319-
320, 352t, 353t, 356-358, 359t
varnish with fluoride in, 351-354,
352t
child development not affected by,
317-318, 348-351
climate and temperature effect on,
326-328, 327t
“contaminant” level in, 332
Dean’s early studies on, 308-309,
310f
Down syndrome not increased by,
316
early studies of cities related to,
211f, 212f, 314-316, 328, 333t
economics (costs) of, 331b, 338-340
fetus affected by, 335, 351
future of, 342
global distribution of, 329-330,
329b, 357-358
legal decisions regarding, 341
McKay’s early assessment of, 307-
308
420 Index
Fluoridation (Continued)
natural occurrence of, 211f, 212f,
307-312, 310f, 312t
non-water sources of, 347-360
optimal levels for, 313-314, 326-
328, 327b, 327t
oral health promotion campaigns
for, 59-60
politics of, 340-342
prenatal, 335, 351
primary dentition affected by, 335-
336
public attitude toward, 340-342
standards and oversight for, 326-
328, 327b, 327t
state and local governments in, 330-
331, 331b, 331t
U.S. standards for, 330-332, 331b,
331t
Fluoride, 287-292, 307-320, 326-342,
347-360
bone mineral density not affected
by, 316-317
dietary supplements of, 289, 349-
351, 350t
enamel mottling caused by, 287-
288, 307-308, 319-320
first-aid for, 317-318
health effects of, 314-318, 318t
historic aspects of, 210, 307-311,
310f
kidney affected by, 313
mortality rate not affected by, 315
multiple sources of, 311-312, 312t,
334, 338, 347, 358-360, 359t
natural occurrence of, 211f, 212f,
307-312, 310f, 312t
optimal intake amount for, 313-
314, 326-328, 327b, 327t
osteosarcoma associated with, 315-
316
physiology of, 287-288, 312-314
plaque and calculus affected by,
207, 207b
toxicities of, 312-313, 317-318, 318t,
353t
Fluorosis, 287-292
crippling skeletal form of, 317, 318t
dietary supplement risk of, 350
distribution of, 211f, 287-288, 307-
311
enamel mottling in, 287-288, 307-
308, 319-320
epidemiologic aspects of, 210f, 211f,
287-292, 307-311, 310f
historic aspects of, 210, 307-311,
310f
measurement of, 210-215
Community Fluorosis Index in,
210, 211f, 212f
Dean’s Fluorosis Index in, 210,
211f, 211t, 212f, 308-309, 310f
Fluorosis (Continued)
Developmental Defects of Dental
Enamel Index in, 213-215,
214t
diagnostic criteria used in, 211b,
212b, 213b, 214t
Fluorosis Risk Index in,
212-213
Thylstrup-Fejerskov index in, 212,
213b, 214f
Tooth Surface Index of Fluorosis
in, 210-211, 212b
physiology in, 287-288
primary vs. permanent dentition in,
287, 307-308, 318-320
risk factors for, 287-288
Fluorosis Risk Index (FRI), 212-213
Fones, Alfred, 6
Food. See Diet.
Fractures, fluoride not affecting, 316-
317
FRI (Fluorosis Risk Index), 212-213
Fructose
in high fructose corn syrup, 383-
384, 383f, 384f
intolerance of, hereditary, 248
FS-T Scale, 195
Future
dental care utilization related to,
22-23
fluoridation in, 342
G health; Oral health; Public
Gels, fluoride, 351-354, 352t
Gender
dental care utilization related to,
18-19, 19f
life expectancy related to, 14-15,
15f
oral cancer related to, 294-296,
295f, 295t, 296f
periodontitis role of, 264f, 266,
266f, 267f
population distribution by, 14-15,
15f
root caries distribution by, 250-251,
250f
Genetic factors
caries affected by, 245
cleft lip and palate with, 299-300
periodontitis role of, 260, 271-272
Geneva declaration, physician’s oath
in, 30b
Geographic regions
dental care utilization related to,
22, 22f
non-U.S., population growth rate
in, 15, 16f
population distribution in, 15-17,
16f
GI (Gingival Index), 203-204
Gies report, dental education in, 5
Gingiva
crevicular fluid of, 206
index related to, 203-204
overhangs of, 273
plaque and calculus under, 207,
207b
root caries and, 198-199
Gingivitis
definition of, 259
epidemiology of, 203-204, 204b
measurement and diagnosis of,
203-204, 204b
natural history of, 259-262, 261b,
262b
periodontitis role of, 259, 262b
plaque control in prevention of,
395
prevalence of, 262-263
Gloves, standard precautions role of,
139
Glycolysis, fluoride inhibition of, 319,
319b
Grainger’s hierarchy scale, 195
Gross domestic product
dental care percentage of, 83, 86f
health care percentage of, 83, 83f
Guild model, 3
H
Hairy leukoplakia, AIDS/HIV with, 142
HDA (Hispanic Dental Association), 9
Health care. See also Dental public
health.
costs of nationally, 83-85, 83f-86f
national insurance proposals for,
107-108
public financing of, 83-84, 83f-84f,
101-108
Health maintenance organizations
(HMOs), 95-97
dental personnel in, 95-96
Health promotion, 50-60
Canadian, 51, 51b
community-based aspects of, 50-53,
51b
definition of, 50-51
oral and dental, 53-60, 56b, 58b
social amenities role in, 51-52, 51b
Stanford Five-Cities study in, 52-53
Healthy People 2010, oral health
objectives in, 55, 56b
Helsinki Declaration, 31
Hepatitis
A, 144
B, 143-145, 144f
C, 143-145, 144f
dentists with, 144-145
incidence of, 143, 144f
non-A, non-B, 144
symptoms of, 143
transmission of, 143-145

High fructose corn syrup, 383-384,
383f, 384f
Hispanic Dental Association (HDA), 9
Hispanics. See also Race.
population demographics for, 17,
17f
History. See also under specific dental
topics.
dental hygiene in, 6-7, 9-10
dentistry in, 3-10
HIV infection, 140-143
dentists with, 142-143
drug treatment for, 141
ethics standards for care in, 28-29
global extent of, 141-142, 141b
legal issues in, 146-147
oral manifestations of, 142-143
periodontitis with, 275-276
T lymphocytes in, 140-141
timeline of, 141
transmission of, 141-142
HMOs (health maintenance
organizations), 95-97
Hopewood House study, 247-248
Hospitals, dental care programs in,
70-71
Host response, in periodontal disease,
260, 262
Human immunodeficiency virus. See
HIV infection.
Human research subjects, ethical
standards for, 31-33, 32b, 33b
I Markers
IADR (International Association for
Dental Research), 32, 32b, 33b
Immunodeficiency
acquired syndrome of, 141-143
HIV infection with, 140-143
periodontal disease model based
on, 260, 262
Income level. See Economic status;
Socioeconomic status.
Index Medicus, journals in, 160-161
Indexes. See also specific index.
epidemiologic measurement using,
187-188, 188b
ideal, 188, 188b
reversible vs. irreversible, 188
Indian Health Service, dental care
financing by, 106
Indigents, 101. See also Poverty.
Individualism
American character role of, 26-28
social responsibility vs., 26-28
Infant
baby bottle caries affecting, 199,
199t, 252
fluoride in formula for, 289
Infection control, 138-147
ADA guidelines for, 139
AIDS/HIV in, 140-143, 141b
Index 421
Infection control (Continued) L
hepatitis in, 143-145, 144f
Laboratory technicians, 113, 122-123
legal issues in, 146-147
Legionnaires’ disease, dental unit
OSHA guidelines for, 139-140
waterline issues in, 147
public perceptions related to, 145-
Leukoplakia
146
hairy, AIDS/HIV with, 142
Institute of Medicine (IOM), public
oral cancer role of, 298, 299
health defined by, 37-38
Life expectancy, U.S. population,
Insurance plans
14-15, 15f
Delta, 90-93, 92f
Literature. See also Journals.
dental care utilization status related
systematic reviews of, 164-170,
to, 22, 23f
164t, 165t, 167b
for-profit, 93-100
textbooks as, 154-155
growing use of in dentistry, 86-88,
Loansome Doc system, 161
87f
London cholera epidemic, 184, 185f
managed care form of, 94-99
administrative services only plan M
in, 98-99
Malocclusion, 300
discount plans in, 98
epidemiologic aspects of, 216-217,
HMO’s in, 95-97
300
personal savings accounts in, 99
race related to, 300
PPO’s in, 97-98
Malthusian theories, 39
not-for-profit, 90-93, 92f
Managed care, 94-99
reimbursement forms used by, 88-
administrative services only plan in,
90
98-99
risk-taking principles guiding,
direct reimbursement in, 98
81-83
discount plans in, 98
Interactive model, 3
historical emergence of, 28
Interdental Bleeding Index, 203-204
HMO’s in, 95-97
Interdental cleaning, 396
personal savings accounts in, 99
International Association for Dental
PPO’s in, 97-98
Research, 32, 32b, 33b
risk assumption in, 96-97
Interval scale, 188b
J gingival crevicular fluid in, 206
periodontitis with, 206
Journals
Masks, standard precautions using,
databases of, 158-161
139
finding reports in, 158-161
Maternal and Child Health Services,
internal vs. external validity in, 157
106
kinds of papers found in, 157-158
McClure, Frank, 313-314
peer review of, 154-155
McKay, Frederick, 307-308
quality assessment related to
Medicaid, 103-106, 103f-105f
clinical decision-making affected
dental care expenditures by, 103-
by, 163-164, 164t, 165t, 168-
106, 103f-105f
170
Medical indigence, definition of, 101
critical reading role in, 156-161,
Medical waste, standard precautions
157b, 159b, 160b
related to, 140
issues in, 156-158, 157b, 159b,
Medicare, 102-103
160b
MEDLINE, 166
presenters qualifications in, 155-
Mercury
156
ADA recommendations related to,
scales designed for, 156-158,
149
157b, 159b, 160b
amalgam restoration leakage of,
systematic reviews of, 164-170,
147-149
164t, 165t, 167b
toxic properties of, 147-149
“throw-aways,” 156
MGI (Modified Gingival Index), 204
K Microbiota. See Bacteria.
Military personnel, dental care for, 107
Kaposi’s sarcoma, AIDS/HIV with, 142
Military service, dentistry career in, 11
Kappa statistic, 189
Mineralization, calculus formation in,
Karlstad Studies, 397-399, 398b
394-395
Kidney, fluoride effects in, 313
Minorities. See Race.
422 Index
Modified Gingival Index (MGI), 204
Molybdenum, low caries levels and,
386
Monosaccharides, in diet, 383-384,
383f, 384f
Morality. See Ethics.
Mortality rate
fluoride not affecting, 315
oral cancer with, 294-296, 295f-
298f, 295t, 296t
Mouthrinses
antiplaque chemicals in, 399-401,
400b
fluoride in, 352t, 353t, 354-355,
359t
N goals for, 54-55, 55b, 56b
National Dental Association (NDA), 8
National Health Service Corps,
scholarship program of, 123-
124
Native Americans, population
demographics for, 17, 17f
NDA. See National Dental Association
(NDA).
Nicotine
addictive quality of, 407, 413b
patches containing, 413b
snuff content of, 409
Nitrosamines, snuff content of, 409
Nominal scale, 188b
Nonprobability, sampling role of,
186-187
Norway, population growth rate in, 16f
Null hypothesis, 180-181
Nuremberg Code, 31
Nurse, dental, 113
Nutrition, 245-246. See also Diet.
caries role of, 245-246, 380-388
oral diseases role of, 273, 380-388
O from, 139-140
Oath, physician’s, 30b
Obesity, soft drinks role in, 382
Occupational Safety and Health
Administration
infection control regulations of,
139-140
standard precautions guidelines
from, 139-140
Office environment, infection control
in. See Infection control.
Oral cancer, 294-302
age and, 295, 295f-297f
distribution of, 294-296, 295f-298f,
295t, 296t
epidemiologic aspects of, 217
gender and, 294-296, 295f, 295t,
296f
leukoplakia related to, 298, 299
mortality rates for, 294-296, 295f-
298f, 295t, 296t
Oral cancer (Continued)
race and, 294-296, 296f-298f, 296t,
298t
risk factors for, 298-299, 407-412
site of occurrence of, 294, 296t
tobacco role in, 298-299, 407-412.
See also Tobacco use.
Oral disease. See Epidemiology; specific
disease.
Oral health. See also Dental public
health; Public health.
indicators of, 43
promotion of, 53-60, 56b
attitudes and knowledge
affecting, 55-57
fluoridation of water in, 59-60
methodology efficacy in, 53-54,
57-58, 58b
other countries role in, 55, 55b
patient education role in, 57-58,
58b
quality of life aspects of, 217-218
surveys of, 43-44
Oral hygiene. See also Plaque.
brushing, flossing, and wood point
use for, 395-397
chemical products used in, 399-
402, 400b
diet and food types affecting, 380-
389
professional treatment for, 397-399,
398b
self-care methods in, 395-397
sugar affecting, 381-389, 381b,
383f, 384f, 388f
Ordinal scale, 188b
OSHA
infection control regulations of,
139-140
standard precautions guidelines
Osteoporosis, periodontitis with, 277
Osteosarcoma, fluoride associated
with, 315-316
P gender role in, 264f, 266, 266f, 267f
Pacific Islanders, population
demographics for, 17, 17f
Papillary hyperplasia, 299
Pathfinder (survey), 44
Pathogens. See Bacteria.
Patients
AIDS/HIV issues related to, 146-147
bad health behaviors of, 135
ethical standards in care of, 28-32,
30b, 32b, 33b
oral health promotion for, 57-58,
58b
personal savings account plans for,
99
research using, 31-33, 32b, 33b
Patients (Continued)
selection of, 28-31, 30b
turnaway of, 28-29, 134, 135, 146
Payment. See Financing; Insurance
plans; Reimbursement.
PDI (Periodontal Disease Index), 204-
205, 205f
Peer review, journals subject to, 154-
155
Pepys, Samuel, 184
Percentile fees, 92, 92f
Periodontal disease, 203-208, 259-
278. See also Periodontitis.
attachment loss in, 204-205, 205f,
206b, 263-266, 264f, 265f
classification of, 260-262, 261b
distribution of, 262-266, 264f, 265f
epidemiologic aspects of, 203-208,
204b, 205f, 206b, 207b
measurement and diagnosis of,
203-208, 204b, 205f, 206b,
207b
gingivitis in, 203-204, 204b, 259-
263, 261b
partial mouth approach to, 204,
207-208
periodontitis in, 204-206, 205f
plaque and calculus in, 207, 207b
treatment criteria in, 206-207,
206b
models of, 260-262, 261b, 262b
natural history of, 260-262, 262b
prediction of, 278
risk factors for, 266-278
severe vs. moderate, 260-262, 261b
Periodontal Disease Index (PDI), 204-
205, 205f
Periodontal Index (PI), 204
Periodontitis, 259-278
bacteria in, 272
cardiovascular disorders with, 276-
277
cytokine marker for, 206
definition of, 259
diabetes mellitus with, 274-275
epidemiology of, 204-206, 205f
genetic factors in, 260, 271-272
HIV infection with, 275-276
incidence of, 264-266
measurement and diagnosis of,
204-206, 205f
natural history of, 260-262, 262b
nutrition and diet in, 273, 380-388
oral hygiene role in, 272
osteoporosis with, 277
plaque role in, 272, 388-389
pregnancy affected by, 277-278
prevalence of, 263
psychosocial stress in, 274
race role in, 266-268, 268f
risk factors for, 266-278

Periodontitis (Continued)
severe vs. moderate, 260-262, 261b
socioeconomic status and, 267,
267f, 269-271, 270f, 271f
systemic disorders affecting, 274-
278
tobacco use role in, 273-274
Personnel. See Dental auxillaries;
Dental hygienists; Dentists.
Peru, population growth rate in, 16f
Physician’s oath, 30b
PI (Periodontal Index), 204
Placebos
ethical standards for use of, 31-32
research studies use of, 179
Plagiarism, 33
Plaque, 303-402
bacteria associated with, 394-395
brushing, flossing, and wood point
use for, 395-397
chemical products used against,
399-402, 400b
control and removal of, 393-402,
398b
approaches to, 395
chemotherapeutic agents for,
399-402, 400b
dietary constraint used in, 387-
389, 388f
fluoride inhibition in, 319, 401-
402
professional treatment for, 397-
399, 398b
public education about, 402
rationale for, 393-394
self-care methods for, 395-397
definition of, 394
ecologic aspects of, 388, 395
epidemiology of, 207, 207b
evolutionary benefits of, 388, 395
measurement and diagnosis of, 207,
207b
natural history of, 394-395
periodontal disease role of, 259-
263, 272, 388-389
pH of, 381, 381b, 387, 388f
Plaque Index, 207, 207b
P-M-A (Papillary-Marginal-Attached)
Index, 203
Pockets
balled and marked probe for, 206,
206b
periodontal attachment loss with,
204-205, 205f, 206b
Politics, fluoridation and, 340-342
Poor Laws, 39-40
Population, 14-23
age distribution of, 15, 15f, 16f,
130-132, 131f, 132f
dental care utilization related to,
18-23, 19f-23f
dentists per 100,000 of
Population (Continued)
other countries, 113, 113b
state distribution as, 115-116, 115t
U.S., 113t
economic distribution in, 17, 17f
ethnic and racial composition of,
17, 17f
gender distribution in, 14-15, 15f
geographic distribution of, 15-17,
16f
other countries, 15, 16f
public health aspects of, 37-39. See
also Public health.
size and growth of, 14-15, 15f, 16f
survey sampling of, 186-187
U.S., 14-18, 15f-17f
Pott, Percival, 184
Poverty
edentulism related to, 227f, 229f
legislated programs in response
to, 27
medically indigent defined in, 101
population distribution of, 17
PPO (preferred provider
organization), 97-98
Preauthorization, insurance plans use
of, 92-93
Precautions. See Standard precautions.
Preeruptive teeth, fluoride in, 287-
288, 318-320, 319b, 349-350
Preferred provider organization
(PPO), 97-98
Pregnancy, periodontitis affecting,
277-278
Primary dentition
def index and, 194-195
fluoridation effects in, 335-336
fluorosis affecting, 287, 307-308,
318-320
sealant use on, 370
Private practice, 10
dental public health goals and, 47
salaried practice vs., 10-12
Probability, sampling role of, 186-187
Probes, periodontal treatment
assessment with, 206, 206b
Procedure codes, insurance plans use
of, 93
Professionalism
characteristics of, 3-4, 4b
definition of, 3
ethics related to. See Ethics.
model types for, 3-4
Profiling, dental providers
undergoing, 77
Prophylactic treatment, oral hygiene
role of, 398-399
Psychosocial factors. See also
Socioeconomic status.
periodontitis affected by, 274
temporomandibular joint
dysfunction with, 301-302
Index 423
Public financing programs
dental care in, 83-85, 85f, 86f, 102-
108, 104f, 105f
health care in, 83-84, 83f-84f, 101-
108, 102f, 103f
Indian Health Service in, 106
Medicaid in, 103-106, 103f-105f
Medicare in, 102-103
Public health, 36-47. See also Dental
public health.
core functions and services in, 38, 38b
definition of, 36-38
development of in U.S., 38-40
epidemics in, 38-39, 40
history of, 39-40
identifying problems in, 38-39
population health in, 37
purpose and practice of, 38b
Public Health Service
dentistry career destination in, 11-12
fluoridation guidelines of, 326-328,
327b, 327t
Public programs. See also Fluoridation;
Social welfare.
dental practice history in, 71-73
fissure sealant use in, 370-372, 371f
Publications. See also Journals.
textbooks as, 154-155
PubMed database, 160
Pulp, caries affecting, 197b
Pyrophosphates, anticalculus effects
of, 401
Q
Quality assurance. See also Scales.
activities aimed at, 76-77
cost control role of, 77-78
dental practice in, 73-78, 74b
on-site evaluation for, 76
recent issues in, 75
structure-process-outcome model
for, 73-74, 74b
terminology of, 73-74, 74b
Quality of life, oral health affecting,
217-218
Questionnaires, oral health telephone
surveys using, 43-44
R
Race
caries distribution by, 240f, 241,
242f
dental care utilization related to, 21-
22
fissure sealant use and, 370, 371f
malocclusion related to, 300
oral cancer related to, 294-296,
296f-298f, 296t, 298t
periodontitis role of, 266-268, 268f
population composition by, 17, 17f
root caries distribution by, 251, 251f
tooth loss related to, 226, 227f
424 Index
Ramfjord teeth, 204-205, 205f
Random allocation, research studies
use of, 178-179
Ratio scale, 188b
Regulation, ethical standards used for,
25-26, 26b, 28-33, 30b, 32b,
33b
Reimbursement
capitation basis in, 89-90
Delta Dental Plans in, 91-93, 92f
direct form of, 98
fee schedules for, 88-89
managed care form of, 98
percentile fees in, 92, 92f
table of allowances in, 88-89
third part plan forms of, 88-90
usual, customary, and reasonable,
88-89
Reliability
examiner attribute of, 180, 189-
190, 190f
negative and positive reversals
affecting, 189-190, 190f
research studies role of, 180, 188b,
189-190, 190f
Research
analytic vs. descriptive, 173, 174b,
176
case-control form for, 176-177
causality and risk criteria for, 173-
176, 175b
critical reading of articles on, 157,
157b, 159b
cross-sectional vs. longitudinal, 176
ecologic (community data) form of,
177
epidemiologic design of, 173-182,
174b, 175b
ethical standards and principles in,
31-33, 32b, 33b
experimental, 177-182
blinding in, 179
choice of population for, 177-178
control groups in, 178-179
duration role in, 180
ethical factors for, 182
examiner reliability in, 180, 189-
190, 190f
field trial vs. clinical trial in, 177-
178
placebo use in, 179
random allocation in, 178-179
statistical significance of, 180-181
human subject standards in, 31-33,
32b, 33b
journal reports on. See Journals.
nonexperimental (survey), 176-177
prospective vs. retrospective, 176
protocol features for, 173, 174b
review board for, 32-33
Reversals, negative and positive, 189-
190, 190f
Reviews of literature. See also
Dentistry, evidence-based.
systematic, 164-170, 164t, 165t,
167b
components of, 166-167
examples of use of, 167-168,
167b
Risk factors, 173-176, 175b
definition of, 175
demographic, 176
exposure role in, 174b, 175, 175b
indicator, marker, and predictive,
175-176
research studies role of, 173-176,
175b
Root caries, 198-199, 198b, 250-251,
250f, 251f
age group with, 250-251, 250f, 251f
gender with, 250-251, 250f
gingival recession with, 198-199
index formula for, 198
race factors and, 251, 251f
S 51b
Saccharin, 385
Safe Drinking Water Act, fluoridation
standards in, 331-332
Salaried practice, 10-11
Saliva, fluoride level in, 320
Sampling
errors in, 186
probability vs. nonprobability form
of, 186-187
survey use of, 186-187
Sarcoma, Kaposi’s, 142
Savings account insurance plans, 99
Scales
caries assessment using, 196-198,
197b
dichotomous, 196-198, 197b
epidemiologic measurement using,
188-189, 188b
journal quality assessment by, 156-
158, 157b, 159b, 160b
potential treatments graded in, 163-
164, 164t, 165t
T-Health, 195-196
types of, 188-189, 188b
SCHIP (State Children’s Health
Insurance Program), 106
Schools. See also Dental education;
Education.
drinking water fluoridation in, 348-
351, 350t
fissure sealant programs in, 370-
372, 371f
Sealants. See Fissure sealants.
SEER (Surveillance, Epidemiology,
and End Results), 42
Selenium, high caries levels and, 386
Self-care, plaque control and removal
by, 395-397
Significant Caries Index (SiC), 195
Smokeless tobacco, 298, 408-412. See
also Tobacco use.
pathologic effects of, 408-410
restrictions placed on, 411-412,
413b
Snow, John, 184, 185f
Snuff. See Smokeless tobacco.
Social Security Act, 101-102
Social welfare
access for everyone challenge in, 33-
34
history of, 26-28
individual vs. public responsibility
in, 26-28
Socioeconomic status
caries distribution and, 233-245,
234t, 235f, 235t, 244f
dental care utilization related to,
20-21, 21f
fluoridation caries reduction and,
333-334, 334f
health promotion role of, 51-52,
periodontitis role of, 267, 267f,
269-271, 270f, 271f
population distribution related
to, 17
Soft drinks
caries role of, 240-250
diet content of, 382-383
marketing of, 382-383
Sorbitol, 382, 385
Specialization, dental practice with,
115
Standard precautions, 138-140
ADA guidelines for, 139
AIDS/HIV prevention by, 142
hepatitis prevention by, 144-145
OSHA regulations for, 139-140
Standards
ethical, 25-26, 26b, 28-33, 30b,
32b, 33b
fluoridation role of
oversight, 326-328, 327b, 327t
state and local, 330-331, 331b,
331t
U.S, 330-332, 331b, 331t
regulatory, 25-26, 26b, 28-33, 30b,
32b, 33b
research principles in, 31-33, 32b,
33b
Stanford Five-Cities study, 52-53
Stannous fluoride, oral hygiene use of,
401
Starches
233-252,381b. See also Sugars.
caries role of, 245-250
cariogenicity of, 381b
complex, 384
enzymatic conversion of, 381b
sugars produced from, 381b

State Children’s Health Insurance,
106
States
dental practice legislation by, 118
dentist distribution in, 115-116,
115t
Statistical significance
research studies role of, 180-182
type I vs. type II error related to,
181-182
Stephan curve, 387, 388f
Stomatologist, definition of, 5
Structure-process-outcome model, 73-
74, 74b
Sucrose, consumption per capita of,
383-384, 383f, 384f
Sugar alcohols, 382, 385-386
Sugars, 233-252, 380-389. See also
Starches.
acidogenicity of, 381b, 387, 388f
caries role of, 245-250, 381-385,
381b, 383f, 384f, 388f
consumption per capita of, 383-
384, 383f, 384f
enzymatic conversion source of,
381b
intake frequency of, 248, 249
intrinsic vs. extrinsic, 381b
invert form of, 385
oral hygiene effects of, 381-389,
381b, 383f, 384f, 388f
Sun Belt, population migration to,
16-17
Surveillance process
active vs. passive, 43
dental public health use of, 42-45,
44b
Surveys
dental public health use of, 43-45,
44b, 186-187
research studies design using, 176-
177, 186-187
sampling of human population for,
186-187
Sweeteners, sugar alcohols as, 382,
385-386
Syria, population growth rate in, 16f
T frequency of use of, 396
T lymphocytes, in AIDS, 140-141
Teaching. See Dental education.
Teeth. See also Edentulism; Primary
dentition; Tooth loss.
preeruptive, fluoride in, 287-288,
318-320, 319b, 349-350
Ramfjord, 204-205, 205f
Temperature, fluoridation affected by,
326-328, 327t
Temporomandibular joint
dysfunction, 300-302
depression related to, 301-302
prevalence of, 301
symptoms of, 300-302
T-Health scale, 195-196
Thylstrup-Fejerskov (TF) index, 212,
213b, 214f
Tobacco use, 298-299, 407-412
control programs for, 410-412, 411b,
413b
Master Settlement Agreement on,
410, 410b
oral cancer role of, 298-299, 407-412
periodontitis role of, 273-274
prevalence of, 408, 409b
quitting difficulties of, 411-412,
413b
risks and consequences of, 407-408
smokeless tobacco in, 298, 408-410
Tooth loss, 223-230. See also
Edentulism.
causes of, 228-230
dental care utilization related to, 20,
20f, 230
gender differences in, 225-226, 228,
229f
historical aspects of, 223-228, 224f,
227f
income status and, 224, 224t, 225,
227f
oral health promotion goals for, 55,
55b, 56b
partial, 226-228, 228f, 229f
patient choice role in, 55, 55b
race and ethnic differences in, 226,
227f
total (edentulous), 224-226, 224f,
224t-226t, 227f
Tooth surface
caries related to, 237
fluoridation effect linked to, 320,
349-350
sealants applied to. See Fissure
sealants.
Tooth Surface Index of Fluorosis
(TSIF), 210-211, 212b
Toothbrushes
interdental cleaning with, 396
method of application of, 396
motivation related to use of, 396-
397
plaque removal methods using,
395-397
powered vs. manual, 167-168, 396
self-care role of, 395-397
types of, 396
Index 425
Toothpastes
anticalculus agents in, 401-402
fluoride in, 289, 319-320, 352t,
353t, 356-358, 359t
Toxicity, of fluoride, 312-313, 317-318,
318t, 353t
Triclosan, antiplaque effects of, 401-
402
Tristan da Cunha study, 247
U
U.S. Public Health Service, career
options in, 11-12
Usual, customary, and reasonable
(UCR) fees, 88-89
V
Varnish, fluoride with, caries
reduction by, 354
Veterans, dental care for, 107
Vipehí4lm study, 248, 248b, 387
Volpe-Manhold Index (VMI), 207
W
Waste, medical, standard precautions
for, 140
Water supply. See also Fluoridation;
Fluoride; Fluorosis.
Dean’s Fluorosis Index role of, 211f,
212f, 310f, 312t
fluoride content of, 211f, 212f, 289,
307-312, 310f, 312t
natural occurrence of, 211f, 212f,
307-312, 310f, 312t
optimal levels for, 326-328, 327b,
327t
school drinking water with, 348-
351, 350t
standards and oversight for, 326-
328, 327b, 327t
Sun Belt migration effect on, 16-17
Waterlines, infection control issues
for, 147
Wood points, plaque removal using,
396
World Dental Federation, 9
World Health Organization,
fluoridation guidelines of,
327
World Medical Association
Geneva declaration of, 30b
Helsinki declaration of, 31
World War II Studies, 247
World Wide Web, journal contents on,
160-161
X
Xylitol, 382, 385-386